Phenotype	Phenotype Details	Title	Abstract	Journal	Year		Author(s)	PMID	Age	Sex	N Range	Units	C57BL/6J	C3H/HeJ	BXH2	BXH3	BXH4	BXH6	BXH7	BXH8	BXH9	BXH10	BXH11	BXH12	BXH14	BXH19

brain weight		"Eye1 and Eye2: gene loci that modulate eye size, lens weight, and retinal area in the mouse."		Invest Ophthalmol Vis Sci	1999		"Zhou G, Williams RW"	10102277	100 days	both		mg			433	441.9	474.6	428.5	459.1	444.9	447.5	441.8	420.1	434.3	424.3	429
body weight		"Eye1 and Eye2: gene loci that modulate eye size, lens weight, and retinal area in the mouse."		Invest Ophthalmol Vis Sci	1999		"Zhou G, Williams RW"	10102277	100 days	both		g			23.2	22.4	25.7	17.4	21.8	23.5	22.3	20.1	21.5	21	19.5	20.6
cerebellum weight				<www.nervenet.org>	2000		"Airey DC, Williams RW"		100 days	both		mg			53.3	60.2	58.6	60.6	58.5	56.9	67.5	56.3	56	57.7	55.3	53.9
eye weight		"Eye1 and Eye2: gene loci that modulate eye size, lens weight, and retinal area in the mouse."		Invest Ophthalmol Vis Sci	1999		"Zhou G, Williams RW"	10102277	100 days	both					17.1	16.3	17.9	16.7	16.7	16.7	15.2	15.4	18.7	19.2	16.3	16.2
hippocampus weight				<www.nervenet.org>	2000		Lu L et al		100 days	both					25.8	25.8	29.8	28.5	27.7	26.6	28.6	29.5	27.5	29.4	24.2	27.4
olfactory bulb weight				<www.nervenet.org>	2000		Williams RW et al		100 days	both					17.2	19.5	18	20.4	17.8	17.2	19.8	17.8	21.4	19.3	19	17.3
forebrain plus mid weight	mean value calculated 7/5/00			<www.nervenet.org>	2000		Williams RW et al		100 days	both					299.3	305.3	331.6	300.8	327	322.6	307.5	314.8	313.7	302.3	289.8	297.4
medulla weight	mean value calculated 7/5/00			<www.nervenet.org>	2000		Williams RW et al		100 days	both					4.3	U	U	U	4.6	3.7	U	3	U	4.7	U	U
hindbrain weight	mean value calculated 7/6/00	"Eye1 and Eye2: gene loci that modulate eye size, lens weight, and retinal area in the mouse."		<www.nervenet.org>	2000		Williams RW et al		100 days	both					42.9	41.5	42.1	42.6	41.3	40.2	47.6	40.8	43.2	41.5	41.3	39.4
lens weight	mean value calculated 7/6/00	"Eye1 and Eye2: gene loci that modulate eye size, lens weight, and retinal area in the mouse."		Invest Ophthalmol Vis Sci	1999		"Zhou G, Williams RW"	10102277	100 days	both					6	5.8	6.1	6	5.6	5.6	5.7	5.2	6.3	5.8	5.7	5.1
retinal area	mean value calculated 7/6/00	"Eye1 and Eye2: gene loci that modulate eye size, lens weight, and retinal area in the mouse."		Invest Ophthalmol Vis Sci	1999		"Zhou G, Williams RW"	10102277	100 days	both		mm^2			17.5	16.8	18	18	17.2	17.3	16.4	15.1	18.8	19.7	17.1	16.3
%CAFC day 7 in S-phase 	strain distribution pattern	Genetic analysis of hemopoietic cell cycling in mice suggests its involvement in organismal life span.	"Normal somatic cells undergo replicative senescence in vitro but the significance of this process in organismic aging remains controversial. We have shown previously that hemopoietic stem cells of common inbred strains of mice vary widely in cycling activity and that this parameter is inversely correlated with strain-dependent mean life span. To assess whether cell cycling and life span are causally related, we searched for quantitative trait loci (QTLs) that contributed to variation of these traits in BXH and BXD recombinant inbred mice. Two QTLs, mapping to exactly the same intervals on chromosomes 7 and 11, were identified that were associated with variation of both cell cycling and life span. The locus on chromosome 11 mapped to the cytokine cluster, a segment that shows synteny with human chromosome 5q, in which deletions are strongly associated with myelodysplastic syndrome. These data indicate that steady-state cell turn-over, here measured in hemopoietic progenitor cells, may have a significant effect on the mean life span of mammals."	FASEB	1999	Apr	"De Haan G, Van Zant G."	10094931	42 - 56 days	female		%	8	31	26.6	0.6	26.1	29.9	0.6	0.7	12	13.1	50.9	9	27	0.6
Baseline ventilatory characteristics of BXH recombinanat inbred strains	Wt	Genetic control of differential baseline breathing pattern.	"The purpose of the present study was to determine the genetic control of baseline breathing pattern by examining the mode of inheritance between two inbred murine strains with differential breathing characteristics. Specifically, the rapid, shallow phenotype of the C57BL/6J (B6) strain is consistently distinct from the slow, deep phenotype of the C3H/HeJ (C3) strain. The response distributions of segregant and nonsegregant progeny were compared with the two progenitor strains to determine the mode of inheritance for each ventilatory characteristic. The BXH recombinant inbred (RI) strains derived from the B6 and C3 progenitors were examined to establish strain distribution patterns for each ventilatory trait. To establish the mode of inheritance, baseline breathing frequency (f), tidal volume, and inspiratory time (TI) were measured five times in each of 178 mature male animals from the two progenitor strains and their progeny by using whole body plethysmography. With respect to f and TI, the two progenitor strains were consistently distinct, and segregation analyses of the inheritance pattern suggest that the most parsimonious genetic model for response distributions of f and TI is a two-loci model. In similar experiments conducted on 82 mature male animals from 12 BXH RI strains, each parental phenotype was represented by one or more of the RI strains. Intermediate phenotypes emerged to confirm the likelihood that parental strain differences in f and TI were determined by more than one locus. Taken together, these studies suggest that the phenotypic difference in baseline respiratory timing between male B6 and C3 mice is best explained by a genetic model that considers at least two loci as major determinants."	J Appl Physiol	1997	Mar	"Tankersley CG, Fitzgerald RS, Levitt RC, Mitzner WA, Ewart SL, Kleeberger SR."	9074977	68 - 96 days	male	10-Apr	g			20.4	26.2	28.7	21.2	28	25.6	25.5	21.3	22.8	20.9	22.9	25.8
Baseline ventilatory characteristics of BXH recombinanat inbred strains	f	Genetic control of differential baseline breathing pattern.	"The purpose of the present study was to determine the genetic control of baseline breathing pattern by examining the mode of inheritance between two inbred murine strains with differential breathing characteristics. Specifically, the rapid, shallow phenotype of the C57BL/6J (B6) strain is consistently distinct from the slow, deep phenotype of the C3H/HeJ (C3) strain. The response distributions of segregant and nonsegregant progeny were compared with the two progenitor strains to determine the mode of inheritance for each ventilatory characteristic. The BXH recombinant inbred (RI) strains derived from the B6 and C3 progenitors were examined to establish strain distribution patterns for each ventilatory trait. To establish the mode of inheritance, baseline breathing frequency (f), tidal volume, and inspiratory time (TI) were measured five times in each of 178 mature male animals from the two progenitor strains and their progeny by using whole body plethysmography. With respect to f and TI, the two progenitor strains were consistently distinct, and segregation analyses of the inheritance pattern suggest that the most parsimonious genetic model for response distributions of f and TI is a two-loci model. In similar experiments conducted on 82 mature male animals from 12 BXH RI strains, each parental phenotype was represented by one or more of the RI strains. Intermediate phenotypes emerged to confirm the likelihood that parental strain differences in f and TI were determined by more than one locus. Taken together, these studies suggest that the phenotypic difference in baseline respiratory timing between male B6 and C3 mice is best explained by a genetic model that considers at least two loci as major determinants."	J Appl Physiol	1997	Mar	"Tankersley CG, Fitzgerald RS, Levitt RC, Mitzner WA, Ewart SL, Kleeberger SR."	9074977	68 - 96 days	male	10-Apr	Hz	2.8	1.8	2..36 	2.62	2.63	2.24	2.59	1.67	2.44	2.71	2.6	3.01	3.42	2.09
Baseline ventilatory characteristics of BXH recombinanat inbred strains	inspiratory time	Genetic control of differential baseline breathing pattern.	"The purpose of the present study was to determine the genetic control of baseline breathing pattern by examining the mode of inheritance between two inbred murine strains with differential breathing characteristics. Specifically, the rapid, shallow phenotype of the C57BL/6J (B6) strain is consistently distinct from the slow, deep phenotype of the C3H/HeJ (C3) strain. The response distributions of segregant and nonsegregant progeny were compared with the two progenitor strains to determine the mode of inheritance for each ventilatory characteristic. The BXH recombinant inbred (RI) strains derived from the B6 and C3 progenitors were examined to establish strain distribution patterns for each ventilatory trait. To establish the mode of inheritance, baseline breathing frequency (f), tidal volume, and inspiratory time (TI) were measured five times in each of 178 mature male animals from the two progenitor strains and their progeny by using whole body plethysmography. With respect to f and TI, the two progenitor strains were consistently distinct, and segregation analyses of the inheritance pattern suggest that the most parsimonious genetic model for response distributions of f and TI is a two-loci model. In similar experiments conducted on 82 mature male animals from 12 BXH RI strains, each parental phenotype was represented by one or more of the RI strains. Intermediate phenotypes emerged to confirm the likelihood that parental strain differences in f and TI were determined by more than one locus. Taken together, these studies suggest that the phenotypic difference in baseline respiratory timing between male B6 and C3 mice is best explained by a genetic model that considers at least two loci as major determinants."	J Appl Physiol	1997	Mar	"Tankersley CG, Fitzgerald RS, Levitt RC, Mitzner WA, Ewart SL, Kleeberger SR."	9074977	68 - 96 days	male	10-Apr	s	0.112	0.188	0.158	0.138	0.126	0.166	0.134	0.19	0.134	0.126	0.143	0.125	0.118	0.154
Baseline ventilatory characteristics of BXH recombinanat inbred strains	VT	Genetic control of differential baseline breathing pattern.	"The purpose of the present study was to determine the genetic control of baseline breathing pattern by examining the mode of inheritance between two inbred murine strains with differential breathing characteristics. Specifically, the rapid, shallow phenotype of the C57BL/6J (B6) strain is consistently distinct from the slow, deep phenotype of the C3H/HeJ (C3) strain. The response distributions of segregant and nonsegregant progeny were compared with the two progenitor strains to determine the mode of inheritance for each ventilatory characteristic. The BXH recombinant inbred (RI) strains derived from the B6 and C3 progenitors were examined to establish strain distribution patterns for each ventilatory trait. To establish the mode of inheritance, baseline breathing frequency (f), tidal volume, and inspiratory time (TI) were measured five times in each of 178 mature male animals from the two progenitor strains and their progeny by using whole body plethysmography. With respect to f and TI, the two progenitor strains were consistently distinct, and segregation analyses of the inheritance pattern suggest that the most parsimonious genetic model for response distributions of f and TI is a two-loci model. In similar experiments conducted on 82 mature male animals from 12 BXH RI strains, each parental phenotype was represented by one or more of the RI strains. Intermediate phenotypes emerged to confirm the likelihood that parental strain differences in f and TI were determined by more than one locus. Taken together, these studies suggest that the phenotypic difference in baseline respiratory timing between male B6 and C3 mice is best explained by a genetic model that considers at least two loci as major determinants."	J Appl Physiol	1997	Mar	"Tankersley CG, Fitzgerald RS, Levitt RC, Mitzner WA, Ewart SL, Kleeberger SR."	9074977	68 - 96 days	male	10-Apr	ml/ g			9.5	6.8	7.5	8.3	7.7	9.7	9	8.6	2.6	3.01	3.42	2.09
Baseline ventilatory characteristics of BXH recombinanat inbred strains	VE	Genetic control of differential baseline breathing pattern.	"The purpose of the present study was to determine the genetic control of baseline breathing pattern by examining the mode of inheritance between two inbred murine strains with differential breathing characteristics. Specifically, the rapid, shallow phenotype of the C57BL/6J (B6) strain is consistently distinct from the slow, deep phenotype of the C3H/HeJ (C3) strain. The response distributions of segregant and nonsegregant progeny were compared with the two progenitor strains to determine the mode of inheritance for each ventilatory characteristic. The BXH recombinant inbred (RI) strains derived from the B6 and C3 progenitors were examined to establish strain distribution patterns for each ventilatory trait. To establish the mode of inheritance, baseline breathing frequency (f), tidal volume, and inspiratory time (TI) were measured five times in each of 178 mature male animals from the two progenitor strains and their progeny by using whole body plethysmography. With respect to f and TI, the two progenitor strains were consistently distinct, and segregation analyses of the inheritance pattern suggest that the most parsimonious genetic model for response distributions of f and TI is a two-loci model. In similar experiments conducted on 82 mature male animals from 12 BXH RI strains, each parental phenotype was represented by one or more of the RI strains. Intermediate phenotypes emerged to confirm the likelihood that parental strain differences in f and TI were determined by more than one locus. Taken together, these studies suggest that the phenotypic difference in baseline respiratory timing between male B6 and C3 mice is best explained by a genetic model that considers at least two loci as major determinants."	J Appl Physiol	1997	Mar	"Tankersley CG, Fitzgerald RS, Levitt RC, Mitzner WA, Ewart SL, Kleeberger SR."	9074977	68 - 96 days	male	10-Apr	ml . min-1 . g-1   			1.35	1.05	1.17	1.1	1.19	0.96	1.32	1.36	1.06	1.14	1.28	1.02
Baseline ventilatory characteristics of BXH recombinanat inbred strains	TI	Genetic control of differential baseline breathing pattern.	"The purpose of the present study was to determine the genetic control of baseline breathing pattern by examining the mode of inheritance between two inbred murine strains with differential breathing characteristics. Specifically, the rapid, shallow phenotype of the C57BL/6J (B6) strain is consistently distinct from the slow, deep phenotype of the C3H/HeJ (C3) strain. The response distributions of segregant and nonsegregant progeny were compared with the two progenitor strains to determine the mode of inheritance for each ventilatory characteristic. The BXH recombinant inbred (RI) strains derived from the B6 and C3 progenitors were examined to establish strain distribution patterns for each ventilatory trait. To establish the mode of inheritance, baseline breathing frequency (f), tidal volume, and inspiratory time (TI) were measured five times in each of 178 mature male animals from the two progenitor strains and their progeny by using whole body plethysmography. With respect to f and TI, the two progenitor strains were consistently distinct, and segregation analyses of the inheritance pattern suggest that the most parsimonious genetic model for response distributions of f and TI is a two-loci model. In similar experiments conducted on 82 mature male animals from 12 BXH RI strains, each parental phenotype was represented by one or more of the RI strains. Intermediate phenotypes emerged to confirm the likelihood that parental strain differences in f and TI were determined by more than one locus. Taken together, these studies suggest that the phenotypic difference in baseline respiratory timing between male B6 and C3 mice is best explained by a genetic model that considers at least two loci as major determinants."	J Appl Physiol	1997	Mar	"Tankersley CG, Fitzgerald RS, Levitt RC, Mitzner WA, Ewart SL, Kleeberger SR."	9074977	68 - 96 days	male	10-Apr	ms			157	138	127	165	133	190	134	125	141	124	118	155
Baseline ventilatory characteristics of BXH recombinanat inbred strains	TE	Genetic control of differential baseline breathing pattern.	"The purpose of the present study was to determine the genetic control of baseline breathing pattern by examining the mode of inheritance between two inbred murine strains with differential breathing characteristics. Specifically, the rapid, shallow phenotype of the C57BL/6J (B6) strain is consistently distinct from the slow, deep phenotype of the C3H/HeJ (C3) strain. The response distributions of segregant and nonsegregant progeny were compared with the two progenitor strains to determine the mode of inheritance for each ventilatory characteristic. The BXH recombinant inbred (RI) strains derived from the B6 and C3 progenitors were examined to establish strain distribution patterns for each ventilatory trait. To establish the mode of inheritance, baseline breathing frequency (f), tidal volume, and inspiratory time (TI) were measured five times in each of 178 mature male animals from the two progenitor strains and their progeny by using whole body plethysmography. With respect to f and TI, the two progenitor strains were consistently distinct, and segregation analyses of the inheritance pattern suggest that the most parsimonious genetic model for response distributions of f and TI is a two-loci model. In similar experiments conducted on 82 mature male animals from 12 BXH RI strains, each parental phenotype was represented by one or more of the RI strains. Intermediate phenotypes emerged to confirm the likelihood that parental strain differences in f and TI were determined by more than one locus. Taken together, these studies suggest that the phenotypic difference in baseline respiratory timing between male B6 and C3 mice is best explained by a genetic model that considers at least two loci as major determinants."	J Appl Physiol	1997	Mar	"Tankersley CG, Fitzgerald RS, Levitt RC, Mitzner WA, Ewart SL, Kleeberger SR."	9074977	68 - 96 days	male	10-Apr	ms			269	246	256	296	256	413	277	253	249	211	177	335
Baseline ventilatory characteristics of BXH recombinanat inbred strains	TI/TT	Genetic control of differential baseline breathing pattern.	"The purpose of the present study was to determine the genetic control of baseline breathing pattern by examining the mode of inheritance between two inbred murine strains with differential breathing characteristics. Specifically, the rapid, shallow phenotype of the C57BL/6J (B6) strain is consistently distinct from the slow, deep phenotype of the C3H/HeJ (C3) strain. The response distributions of segregant and nonsegregant progeny were compared with the two progenitor strains to determine the mode of inheritance for each ventilatory characteristic. The BXH recombinant inbred (RI) strains derived from the B6 and C3 progenitors were examined to establish strain distribution patterns for each ventilatory trait. To establish the mode of inheritance, baseline breathing frequency (f), tidal volume, and inspiratory time (TI) were measured five times in each of 178 mature male animals from the two progenitor strains and their progeny by using whole body plethysmography. With respect to f and TI, the two progenitor strains were consistently distinct, and segregation analyses of the inheritance pattern suggest that the most parsimonious genetic model for response distributions of f and TI is a two-loci model. In similar experiments conducted on 82 mature male animals from 12 BXH RI strains, each parental phenotype was represented by one or more of the RI strains. Intermediate phenotypes emerged to confirm the likelihood that parental strain differences in f and TI were determined by more than one locus. Taken together, these studies suggest that the phenotypic difference in baseline respiratory timing between male B6 and C3 mice is best explained by a genetic model that considers at least two loci as major determinants."	J Appl Physiol	1997	Mar	"Tankersley CG, Fitzgerald RS, Levitt RC, Mitzner WA, Ewart SL, Kleeberger SR."	9074977	68 - 96 days	male	10-Apr	%			36.3	35.9	33.4	35.7	34.5	31.6	31.9	33.4	36.1	37.4	40	31.8
Correlation between HO - 1 mRNA induction with MM-LDL in ECs and aortic atherosclerotic lesions 	Aortic Lesions	Determinants of atherosclerosis susceptibility in the C3H and C57BL/6 mouse model: evidence for involvement of endothelial cells but not blood cells or cholesterol metabolism.	"Lipids, monocytes, and arterial wall cells are primary components involved in atherogenesis. Using the inbred mouse strains C57BL/6J (B6) and C3H/HeJ (C3H), which have been extensively studied as models of the genetic control of diet-induced atherosclerosis, we examined which of these components determine genetic susceptibility. To test whether dietary responsiveness is involved, a congenic strain of C3H carrying an apoE-null allele (apoE(-/-)) was constructed. Although C3H.apoE(-/-) mice had higher plasma cholesterol levels, they developed much smaller lesions than their B6.apoE(-/-) counterpart on either chow or Western diets. Reciprocal bone marrow transplantation between the strains, with congenics carrying the same H-2 haplotype, was performed to examine the role of monocytes. The atherosclerosis susceptibility was not altered in the recipient mice, indicating that variations in monocyte function were not involved. Endothelial cells isolated from the aorta of B6 mice exhibited a dramatic induction of monocyte chemotactic protein-1, macrophage colony-stimulating factor, vascular cell adhesion molecule-1, and heme oxygenase-1 in response to minimally modified LDL, whereas endothelial cells from C3H mice showed little or no induction. In a set of recombinant inbred strains derived from the B6 and C3H parental strains, endothelial responses to minimally modified LDL cosegregated with aortic lesion size. These data provide strong evidence that endothelial cells, but not monocytes or plasma lipid levels, account for the difference in susceptibility to atherosclerosis between the 2 mouse strains."	Circulation Research	2000	May	"Shi W, Wang NJ, Shih DM, Sun VZ, Wang X, Lusis AJ"	10827138	105 days	both	5-Feb	mm2	25000	840	42000	---	680	---	---	---	430	2500	8500	--	--	25000
Correlation between HO - 1 mRNA induction with MM-LDL in ECs and aortic atherosclerotic lesions 	HO - 1induction (Fe - LDL: R= 0.57; P= 0.0001)	Determinants of atherosclerosis susceptibility in the C3H and C57BL/6 mouse model: evidence for involvement of endothelial cells but not blood cells or cholesterol metabolism.	"Lipids, monocytes, and arterial wall cells are primary components involved in atherogenesis. Using the inbred mouse strains C57BL/6J (B6) and C3H/HeJ (C3H), which have been extensively studied as models of the genetic control of diet-induced atherosclerosis, we examined which of these components determine genetic susceptibility. To test whether dietary responsiveness is involved, a congenic strain of C3H carrying an apoE-null allele (apoE(-/-)) was constructed. Although C3H.apoE(-/-) mice had higher plasma cholesterol levels, they developed much smaller lesions than their B6.apoE(-/-) counterpart on either chow or Western diets. Reciprocal bone marrow transplantation between the strains, with congenics carrying the same H-2 haplotype, was performed to examine the role of monocytes. The atherosclerosis susceptibility was not altered in the recipient mice, indicating that variations in monocyte function were not involved. Endothelial cells isolated from the aorta of B6 mice exhibited a dramatic induction of monocyte chemotactic protein-1, macrophage colony-stimulating factor, vascular cell adhesion molecule-1, and heme oxygenase-1 in response to minimally modified LDL, whereas endothelial cells from C3H mice showed little or no induction. In a set of recombinant inbred strains derived from the B6 and C3H parental strains, endothelial responses to minimally modified LDL cosegregated with aortic lesion size. These data provide strong evidence that endothelial cells, but not monocytes or plasma lipid levels, account for the difference in susceptibility to atherosclerosis between the 2 mouse strains."	Circulation Research	2000	May	"Shi W, Wang NJ, Shih DM, Sun VZ, Wang X, Lusis AJ"	10827138	105 days	both	5-Feb	fold (with multiple values)	"10.6, 9.6, 7.5, 7.2, 2.5"	"3.4, 2.5, 2.0"	---	---	"2.8, 1.3, 1.0"	---	---	"7.3, 7.0"	"2.5, 1.3"	"6.7, 4.9, 4.4"	"7.9, 3.7, 3.1"	---	---	"9.1, 4.8, 4.0"
Total BAL recovered from BXH RI mice	72 hr exposure to 0.3 ppm O3	Genetic susceptibility to ozone-induced lung hyperpermeability: role of toll-like receptor 4.	"The pollutant ozone (O(3)) induces lung hyperpermeability and inflammation in humans and animal models. Among inbred strains of mice, there is a 3-fold difference in total protein (a marker of permeability) recovered in bronchoalveolar lavage (BAL) fluid after a 72-h exposure to 0.3 ppm O(3). To determine the chromosomal locations of susceptibility genes, we performed a genome screen using recombinant inbred (RI) strains of mice derived from O(3)-susceptible C57BL/6J (B6) and O(3)-resistant C3H/HeJ (HeJ) progenitors. Each RI strain was phenotyped for O(3)-induced hyperpermeability, and linkage was assessed for 558 markers using Map Manager QTb27. A significant quantitative trait locus (QTL) was identified on chromosome 4. The likelihood ratio chi(2) statistic (16.6) for the peak of the QTL was greater than the significance threshold (16.3) determined empirically by permutation test. This QTL contains a candidate gene, Toll-like receptor 4 (Tlr4 ), that recently has been implicated in innate immunity and endotoxin susceptibility. The amount of the total trait variance explained by the QTL at Tlr4, the gene with the highest likelihood ratio statistic in the QTL, was approximately 70%. To test the role of Tlr4 in O(3)-induced hyperpermeability, BAL protein responses to O(3) were compared in C3H/HeOuJ (OuJ) and HeJ mice that differ only at a polymorphism in the coding region of Tlr4. Significantly greater protein concentrations (430 +/- 35 &mgr;g/ml) were found in OuJ mice compared with HeJ mice (258 +/- 18 &mgr;g/ml) after exposure to O(3). Furthermore, reverse transcriptase/polymerase chain reaction analysis demonstrated differential expression of Tlr4 message levels between HeJ and OuJ mice after O(3) exposure. Together, results indicate that a QTL on mouse chromosome 4 explains a significant portion of the genetic variance in O(3)-induced hyperpermeability, and support a role for Tlr4 as a strong candidate susceptibility gene."	Am J Respir Cell Mol Biol	2000	May	"Kleeberger SR, Reddy S, Zhang LY, Jedlicka AE"	10783135	42 - 56 days	both	16-Jun	mg/ ml	525	315	330	220	330	160	280	295	320	530	715	160	455	525
PMNÕs (x103/mL BAL return)	Mean +/ - SE	Genetic susceptibility to ozone-induced lung hyperpermeability: role of toll-like receptor 4.	"The pollutant ozone (O(3)) induces lung hyperpermeability and inflammation in humans and animal models. Among inbred strains of mice, there is a 3-fold difference in total protein (a marker of permeability) recovered in bronchoalveolar lavage (BAL) fluid after a 72-h exposure to 0.3 ppm O(3). To determine the chromosomal locations of susceptibility genes, we performed a genome screen using recombinant inbred (RI) strains of mice derived from O(3)-susceptible C57BL/6J (B6) and O(3)-resistant C3H/HeJ (HeJ) progenitors. Each RI strain was phenotyped for O(3)-induced hyperpermeability, and linkage was assessed for 558 markers using Map Manager QTb27. A significant quantitative trait locus (QTL) was identified on chromosome 4. The likelihood ratio chi(2) statistic (16.6) for the peak of the QTL was greater than the significance threshold (16.3) determined empirically by permutation test. This QTL contains a candidate gene, Toll-like receptor 4 (Tlr4 ), that recently has been implicated in innate immunity and endotoxin susceptibility. The amount of the total trait variance explained by the QTL at Tlr4, the gene with the highest likelihood ratio statistic in the QTL, was approximately 70%. To test the role of Tlr4 in O(3)-induced hyperpermeability, BAL protein responses to O(3) were compared in C3H/HeOuJ (OuJ) and HeJ mice that differ only at a polymorphism in the coding region of Tlr4. Significantly greater protein concentrations (430 +/- 35 &mgr;g/ml) were found in OuJ mice compared with HeJ mice (258 +/- 18 &mgr;g/ml) after exposure to O(3). Furthermore, reverse transcriptase/polymerase chain reaction analysis demonstrated differential expression of Tlr4 message levels between HeJ and OuJ mice after O(3) exposure. Together, results indicate that a QTL on mouse chromosome 4 explains a significant portion of the genetic variance in O(3)-induced hyperpermeability, and support a role for Tlr4 as a strong candidate susceptibility gene."	Am J Respir Cell Mol Biol	2000	May	"Kleeberger SR, Reddy S, Zhang LY, Jedlicka AE"	10783135	42 - 56 days	both	16-Jun		10.1	2.4	2.8	15.3	2.1	1.7	2.3	13.2	1.6	2.8	1.3	2.7	10.8	1.9
PMNÕs (x103/mL BAL return)	Range	Genetic susceptibility to ozone-induced lung hyperpermeability: role of toll-like receptor 4.	"The pollutant ozone (O(3)) induces lung hyperpermeability and inflammation in humans and animal models. Among inbred strains of mice, there is a 3-fold difference in total protein (a marker of permeability) recovered in bronchoalveolar lavage (BAL) fluid after a 72-h exposure to 0.3 ppm O(3). To determine the chromosomal locations of susceptibility genes, we performed a genome screen using recombinant inbred (RI) strains of mice derived from O(3)-susceptible C57BL/6J (B6) and O(3)-resistant C3H/HeJ (HeJ) progenitors. Each RI strain was phenotyped for O(3)-induced hyperpermeability, and linkage was assessed for 558 markers using Map Manager QTb27. A significant quantitative trait locus (QTL) was identified on chromosome 4. The likelihood ratio chi(2) statistic (16.6) for the peak of the QTL was greater than the significance threshold (16.3) determined empirically by permutation test. This QTL contains a candidate gene, Toll-like receptor 4 (Tlr4 ), that recently has been implicated in innate immunity and endotoxin susceptibility. The amount of the total trait variance explained by the QTL at Tlr4, the gene with the highest likelihood ratio statistic in the QTL, was approximately 70%. To test the role of Tlr4 in O(3)-induced hyperpermeability, BAL protein responses to O(3) were compared in C3H/HeOuJ (OuJ) and HeJ mice that differ only at a polymorphism in the coding region of Tlr4. Significantly greater protein concentrations (430 +/- 35 &mgr;g/ml) were found in OuJ mice compared with HeJ mice (258 +/- 18 &mgr;g/ml) after exposure to O(3). Furthermore, reverse transcriptase/polymerase chain reaction analysis demonstrated differential expression of Tlr4 message levels between HeJ and OuJ mice after O(3) exposure. Together, results indicate that a QTL on mouse chromosome 4 explains a significant portion of the genetic variance in O(3)-induced hyperpermeability, and support a role for Tlr4 as a strong candidate susceptibility gene."	Am J Respir Cell Mol Biol	2000	May	"Kleeberger SR, Reddy S, Zhang LY, Jedlicka AE"	10783135	42 - 56 days	both	16-Jun		7.2 - 14.5	0.5 - 4.1	0.5 - 7.4	7.5 - 18.5	0.4 - 7.6	0.4 - 7.6	7.9 - 24.2	0.4 - 2.9	1.0 - 4.6	0.2 - 3.4	0.2 - 3.4	0.7 - 5.5	6.2 - 18.1	0.5 - 3.3
Cell number and brain weights in BXH strains	Mean  +/ - SEM	Natural variation in neuron number in mice is linked to a major quantitative trait locus on Chr 11.	"Common genetic polymorphisms-as opposed to rare mutations-generate almost all heritable differences in the size and structure of the CNS. Surprisingly, these normal variants have not previously been mapped or cloned in any vertebrate species. In a recent paper (), we suggested that much of the variation in retinal ganglion cell number in mice, and the striking bimodality of strain averages, are caused by one or two quantitative trait loci (QTLs). To test this idea, and to map genes linked to this variable and highly heritable quantitative trait, we have counted ganglion cells in 38 recombinant inbred strains (BXD and BXH) derived from parental strains that have high and low cell numbers. A genome-wide search using simple and composite interval-mapping techniques revealed a major QTL on chromosome (Chr) 11 in a 3 cM interval between Hoxb and Krt1 (LOD = 6.8; genome-wide p = 0.001) and possible subsidiary QTLs on Chr 2 and Chr 8. The Chr 11 locus, neuron number control 1 (Nnc1), accounts for one third of the genetic variance among BXH strains and more than half of that among BXD strains, but Nnc1 has no known effects on brain weight, eye weight, or total retinal cell number. Three strong candidate genes have been mapped previously to the same region as Nnc1. These genes-Rara, Thra, and Erbb2- encode receptors for retinoic acid, thyroxine, and neuregulin, respectively. Each receptor is expressed in the retina during development, and their ligands affect the proliferation or survival of retinal cells."	J Neurosci	1998	Jan	"Williams RW, Strom RC, Goldowitz D."	9412494		both	9-Apr	1000x	55.4	67	64.6	63	66.9	52.3	56.5	62.4	57.5	56.2	55	69.5	65.6	55.3
Cell number and brain weights in BXH strains	Type	Natural variation in neuron number in mice is linked to a major quantitative trait locus on Chr 11.	"Common genetic polymorphisms-as opposed to rare mutations-generate almost all heritable differences in the size and structure of the CNS. Surprisingly, these normal variants have not previously been mapped or cloned in any vertebrate species. In a recent paper (), we suggested that much of the variation in retinal ganglion cell number in mice, and the striking bimodality of strain averages, are caused by one or two quantitative trait loci (QTLs). To test this idea, and to map genes linked to this variable and highly heritable quantitative trait, we have counted ganglion cells in 38 recombinant inbred strains (BXD and BXH) derived from parental strains that have high and low cell numbers. A genome-wide search using simple and composite interval-mapping techniques revealed a major QTL on chromosome (Chr) 11 in a 3 cM interval between Hoxb and Krt1 (LOD = 6.8; genome-wide p = 0.001) and possible subsidiary QTLs on Chr 2 and Chr 8. The Chr 11 locus, neuron number control 1 (Nnc1), accounts for one third of the genetic variance among BXH strains and more than half of that among BXD strains, but Nnc1 has no known effects on brain weight, eye weight, or total retinal cell number. Three strong candidate genes have been mapped previously to the same region as Nnc1. These genes-Rara, Thra, and Erbb2- encode receptors for retinoic acid, thyroxine, and neuregulin, respectively. Each receptor is expressed in the retina during development, and their ligands affect the proliferation or survival of retinal cells."	J Neurosci	1998	Jan	"Williams RW, Strom RC, Goldowitz D."	9412494		both			L	H	H	I	H	L	I	I	I	I	L	H	H	L
Cell number and brain weights in BXH strains	Brain	Natural variation in neuron number in mice is linked to a major quantitative trait locus on Chr 11.	"Common genetic polymorphisms-as opposed to rare mutations-generate almost all heritable differences in the size and structure of the CNS. Surprisingly, these normal variants have not previously been mapped or cloned in any vertebrate species. In a recent paper (), we suggested that much of the variation in retinal ganglion cell number in mice, and the striking bimodality of strain averages, are caused by one or two quantitative trait loci (QTLs). To test this idea, and to map genes linked to this variable and highly heritable quantitative trait, we have counted ganglion cells in 38 recombinant inbred strains (BXD and BXH) derived from parental strains that have high and low cell numbers. A genome-wide search using simple and composite interval-mapping techniques revealed a major QTL on chromosome (Chr) 11 in a 3 cM interval between Hoxb and Krt1 (LOD = 6.8; genome-wide p = 0.001) and possible subsidiary QTLs on Chr 2 and Chr 8. The Chr 11 locus, neuron number control 1 (Nnc1), accounts for one third of the genetic variance among BXH strains and more than half of that among BXD strains, but Nnc1 has no known effects on brain weight, eye weight, or total retinal cell number. Three strong candidate genes have been mapped previously to the same region as Nnc1. These genes-Rara, Thra, and Erbb2- encode receptors for retinoic acid, thyroxine, and neuregulin, respectively. Each receptor is expressed in the retina during development, and their ligands affect the proliferation or survival of retinal cells."	J Neurosci	1998	Jan	"Williams RW, Strom RC, Goldowitz D."	9412494		both	13-Mar	mg	475	427	431	442	465	455	471	437	457	455	431	432	432	436
Cell number and brain weights in BXH strains	Residual Cells	Natural variation in neuron number in mice is linked to a major quantitative trait locus on Chr 11.	"Common genetic polymorphisms-as opposed to rare mutations-generate almost all heritable differences in the size and structure of the CNS. Surprisingly, these normal variants have not previously been mapped or cloned in any vertebrate species. In a recent paper (), we suggested that much of the variation in retinal ganglion cell number in mice, and the striking bimodality of strain averages, are caused by one or two quantitative trait loci (QTLs). To test this idea, and to map genes linked to this variable and highly heritable quantitative trait, we have counted ganglion cells in 38 recombinant inbred strains (BXD and BXH) derived from parental strains that have high and low cell numbers. A genome-wide search using simple and composite interval-mapping techniques revealed a major QTL on chromosome (Chr) 11 in a 3 cM interval between Hoxb and Krt1 (LOD = 6.8; genome-wide p = 0.001) and possible subsidiary QTLs on Chr 2 and Chr 8. The Chr 11 locus, neuron number control 1 (Nnc1), accounts for one third of the genetic variance among BXH strains and more than half of that among BXD strains, but Nnc1 has no known effects on brain weight, eye weight, or total retinal cell number. Three strong candidate genes have been mapped previously to the same region as Nnc1. These genes-Rara, Thra, and Erbb2- encode receptors for retinoic acid, thyroxine, and neuregulin, respectively. Each receptor is expressed in the retina during development, and their ligands affect the proliferation or survival of retinal cells."	J Neurosci	1998	Jan	"Williams RW, Strom RC, Goldowitz D."	9412494		both	9-Apr	cells 1000x	---	---	2.48	2.2	8.86	-6.94	-0.82	1	-1.5	-3.04	-7.12	7.5	.3.60	-6.22
Correlation between HO - 1 mRNA induction with MM-LDL in ECs and aortic atherosclerotic lesions 	HO - 1 induction (Cu - LDL: R= 0.79; P= 0.0013	Determinants of atherosclerosis susceptibility in the C3H and C57BL/6 mouse model: evidence for involvement of endothelial cells but not blood cells or cholesterol metabolism.	"Lipids, monocytes, and arterial wall cells are primary components involved in atherogenesis. Using the inbred mouse strains C57BL/6J (B6) and C3H/HeJ (C3H), which have been extensively studied as models of the genetic control of diet-induced atherosclerosis, we examined which of these components determine genetic susceptibility. To test whether dietary responsiveness is involved, a congenic strain of C3H carrying an apoE-null allele (apoE(-/-)) was constructed. Although C3H.apoE(-/-) mice had higher plasma cholesterol levels, they developed much smaller lesions than their B6.apoE(-/-) counterpart on either chow or Western diets. Reciprocal bone marrow transplantation between the strains, with congenics carrying the same H-2 haplotype, was performed to examine the role of monocytes. The atherosclerosis susceptibility was not altered in the recipient mice, indicating that variations in monocyte function were not involved. Endothelial cells isolated from the aorta of B6 mice exhibited a dramatic induction of monocyte chemotactic protein-1, macrophage colony-stimulating factor, vascular cell adhesion molecule-1, and heme oxygenase-1 in response to minimally modified LDL, whereas endothelial cells from C3H mice showed little or no induction. In a set of recombinant inbred strains derived from the B6 and C3H parental strains, endothelial responses to minimally modified LDL cosegregated with aortic lesion size. These data provide strong evidence that endothelial cells, but not monocytes or plasma lipid levels, account for the difference in susceptibility to atherosclerosis between the 2 mouse strains."	Circulation Research	2000	May	"Shi W, Wang NJ, Shih DM, Sun VZ, Wang X, Lusis AJ"	10827138	105 days	both	5-Feb	fold (with multiple values)	"8.8, 8.1, 4.8, 3.5, 2.0"	"2.0, 1.7, 1.4"	---	---	"1.9, 1.5, 1.4"	---	---	"11.3, 8.6, 4.6"	"4.4, 1.4, 1.3"	"3.0, 2.5"	"4.0, 2.5"	---	---	"7.5, 5.2"
BXH RI strains segregate into at least three distinct phenotypes	Survival	Genetic characterization of strain differences in the ability to mediate CD40/CD28-independent rejection of skin allografts.	"Simultaneous blockade of the CD40 and CD28 T cell costimulatory pathways effectively promotes skin allograft survival in C3H/HeJ mice, extending median survival times (MSTs) beyond 100 days. This strategy is markedly less effective in C57BL/6 mice, with MSTs ranging between 20 and 30 days. In this study, we investigate the underlying genetic causes of these distinct phenotypes. Using H-2 congenic mice, we show that the genetic basis for the varied responses between these two strains is independent of the H-2 locus and T cell precursor frequency. C57BL/6 mice treated with costimulation blockade are able to generate allospecific CTL- and IFN-gamma-producing T cells within 3-4 wk posttransplant, whereas mice with a C3H background generate neither CTL- nor IFN-gamma-producing cells. Thus, differences appear to be in the generation of the immune response and not T cell homing. Strain differences in costimulation blockade-induced hyporesponsiveness persist in the absence of CD4(+) T cells, implying a direct effect on CD8(+) T cells. We demonstrate that genetic differences are important in cells of hemopoietic origin and that the costimulation blockade-resistant phenotype is dominant. Analysis of BXH recombinant inbred strains indicates that multiple loci contribute to the phenotype, and that the blockade resistance loci are preliminarily linked to 17 markers on four chromosomes. We conclude that strain variation in allograft MSTs following CD40/CD28 blockade results from the ability of CD8(+) T cells in some strains to use alternative modes of costimulation to mount an effective alloresponse."	 J Immunol	2000	Dec	"Williams MA, Trambley J, Ha J, Adams AB, Durham MM, Rees P, Cowan SR, Pearson TC, Larsen CP."	11120808				days	"17, 18, 19, 20, 22"	"17, 100, 110, >110, >110"	"25, 34, 41, 48"	">110, >110, >110, >110, >110"	"33, 35, 50, 64, 64"	"14, 39, 50, 50, 53"	"53, 53, 68, 95"	"28, 32, 36, 50, >65"	"95, >110, >110, >110, >110"	"18, 23, 26, 27, 50"	"14, 16"	"23, 59, 59, 98"	"14, 14, 20, 26, 95"	">110, >110"
BXH RI strains segregate into at least three distinct phenotypes	MST	Genetic characterization of strain differences in the ability to mediate CD40/CD28-independent rejection of skin allografts.	"Simultaneous blockade of the CD40 and CD28 T cell costimulatory pathways effectively promotes skin allograft survival in C3H/HeJ mice, extending median survival times (MSTs) beyond 100 days. This strategy is markedly less effective in C57BL/6 mice, with MSTs ranging between 20 and 30 days. In this study, we investigate the underlying genetic causes of these distinct phenotypes. Using H-2 congenic mice, we show that the genetic basis for the varied responses between these two strains is independent of the H-2 locus and T cell precursor frequency. C57BL/6 mice treated with costimulation blockade are able to generate allospecific CTL- and IFN-gamma-producing T cells within 3-4 wk posttransplant, whereas mice with a C3H background generate neither CTL- nor IFN-gamma-producing cells. Thus, differences appear to be in the generation of the immune response and not T cell homing. Strain differences in costimulation blockade-induced hyporesponsiveness persist in the absence of CD4(+) T cells, implying a direct effect on CD8(+) T cells. We demonstrate that genetic differences are important in cells of hemopoietic origin and that the costimulation blockade-resistant phenotype is dominant. Analysis of BXH recombinant inbred strains indicates that multiple loci contribute to the phenotype, and that the blockade resistance loci are preliminarily linked to 17 markers on four chromosomes. We conclude that strain variation in allograft MSTs following CD40/CD28 blockade results from the ability of CD8(+) T cells in some strains to use alternative modes of costimulation to mount an effective alloresponse."	 J Immunol	2000	Dec	"Williams MA, Trambley J, Ha J, Adams AB, Durham MM, Rees P, Cowan SR, Pearson TC, Larsen CP."	11120808					19	110	34	>110	50	50	53	36	>110	26	16	59	20	>110
Origin of locus in BXH RI strain	Mrv1	Frequent disruption of the Nf1 gene by a novel murine AIDS virus-related provirus in BXH-2 murine myeloid lymphomas.	"Evi-2, a common site of viral integration in BXH-2 myeloid lymphomas, is located within a large intron of the Nf1 tumor suppressor gene. Viral integration at Evi-2 appears to induce disease by disrupting normal Nf1 expression. During our attempts to characterize the nature of the proviruses located at Evi-2, we found that approximately half of the proviruses were defective nonecotropic proviruses (A. M. Buchberg, H. G. Bedigian, N. A. Jenkins, and N. G. Copeland, Mol. Cell. Biol. 10:4658-4666, 1990). This was surprising, since most proviruses characterized at other BXH-2 common integration sites are full-length ecotropic viruses. In the studies described here, we found that this defective provirus carries two large deletions, one in pol and one in env, and is structurally related to another murine retrovirus, the murine AIDS retrovirus. By using oligonucleotide probes specific for this defective provirus, designated MRV, we showed that MRV-related proviruses are carried as endogenous germ line proviruses in most inbred strains. In addition, we identified the endogenous MRV provirus that gives rise to the defective proviruses identified at Evi-2. We present a model that accounts for the positive selection of MRV proviruses at Evi-2, which may allow selective identification of common viral integration sites harboring tumor suppressor genes."	J Virol	1995	Nov	"Cho BC, Shaughnessy JD Jr, Largaespada DA, Bedigian HG, Buchberg AM, Jenkins NA, Copeland NG."	7474134				"B, C57CL/6J; H, C3H/HeJ"			B	B	H	B	H	B	H	H	H	B	B	H
Origin of locus in BXH RI strain	Mrv2	Frequent disruption of the Nf1 gene by a novel murine AIDS virus-related provirus in BXH-2 murine myeloid lymphomas.	"Evi-2, a common site of viral integration in BXH-2 myeloid lymphomas, is located within a large intron of the Nf1 tumor suppressor gene. Viral integration at Evi-2 appears to induce disease by disrupting normal Nf1 expression. During our attempts to characterize the nature of the proviruses located at Evi-2, we found that approximately half of the proviruses were defective nonecotropic proviruses (A. M. Buchberg, H. G. Bedigian, N. A. Jenkins, and N. G. Copeland, Mol. Cell. Biol. 10:4658-4666, 1990). This was surprising, since most proviruses characterized at other BXH-2 common integration sites are full-length ecotropic viruses. In the studies described here, we found that this defective provirus carries two large deletions, one in pol and one in env, and is structurally related to another murine retrovirus, the murine AIDS retrovirus. By using oligonucleotide probes specific for this defective provirus, designated MRV, we showed that MRV-related proviruses are carried as endogenous germ line proviruses in most inbred strains. In addition, we identified the endogenous MRV provirus that gives rise to the defective proviruses identified at Evi-2. We present a model that accounts for the positive selection of MRV proviruses at Evi-2, which may allow selective identification of common viral integration sites harboring tumor suppressor genes."	J Virol	1995	Nov	"Cho BC, Shaughnessy JD Jr, Largaespada DA, Bedigian HG, Buchberg AM, Jenkins NA, Copeland NG."	7474134				"B, C57CL/6J; H, C3H/HeJ"			B	B	B	H	B	B	B	H	B	H	H	B
Origin of locus in BXH RI strain	Mrv3	Frequent disruption of the Nf1 gene by a novel murine AIDS virus-related provirus in BXH-2 murine myeloid lymphomas.	"Evi-2, a common site of viral integration in BXH-2 myeloid lymphomas, is located within a large intron of the Nf1 tumor suppressor gene. Viral integration at Evi-2 appears to induce disease by disrupting normal Nf1 expression. During our attempts to characterize the nature of the proviruses located at Evi-2, we found that approximately half of the proviruses were defective nonecotropic proviruses (A. M. Buchberg, H. G. Bedigian, N. A. Jenkins, and N. G. Copeland, Mol. Cell. Biol. 10:4658-4666, 1990). This was surprising, since most proviruses characterized at other BXH-2 common integration sites are full-length ecotropic viruses. In the studies described here, we found that this defective provirus carries two large deletions, one in pol and one in env, and is structurally related to another murine retrovirus, the murine AIDS retrovirus. By using oligonucleotide probes specific for this defective provirus, designated MRV, we showed that MRV-related proviruses are carried as endogenous germ line proviruses in most inbred strains. In addition, we identified the endogenous MRV provirus that gives rise to the defective proviruses identified at Evi-2. We present a model that accounts for the positive selection of MRV proviruses at Evi-2, which may allow selective identification of common viral integration sites harboring tumor suppressor genes."	J Virol	1995	Nov	"Cho BC, Shaughnessy JD Jr, Largaespada DA, Bedigian HG, Buchberg AM, Jenkins NA, Copeland NG."	7474134				"B, C57CL/6J; H, C3H/HeJ"			B	H	H	B	B	H	B	H	B	B	B	H
The prevalence of DCC in BXH strains and the correspondence of this phenotype with the parental genotype for microsatellite markers typed on proximal chromosome 7	"D7Mit294, D7Mit266"	A locus on chromosome 7 determines myocardial cell necrosis and calcification (dystrophic cardiac calcinosis) in mice.	"Dystrophic cardiac calcinosis, an age-related cardiomyopathy that occurs among certain inbred strains of mice, involves myocardial injury, necrosis, and calcification. Using a complete linkage map approach and quantitative trait locus analysis, we sought to identify genetic loci determining dystrophic cardiac calcinosis in an F2 intercross of resistant C57BL/6J and susceptible C3H/HeJ inbred strains. We identified a single major locus, designated Dyscalc, located on proximal chromosome 7 in a region syntenic with human chromosomes 19q13 and 11p15. The statistical significance of Dyscalc (logarithm of odds score 14.6) was tested by analysis of permuted trait data. Analysis of BxH recombinant inbred strains confirmed the mapping position. The inheritance pattern indicated that this locus influences susceptibility of cells both to enter necrosis and to subsequently undergo calcification."	Proc Natl Acad Sci U S A 	1996	May	"Ivandic BT, Qiao JH, Machleder D, Liao F, Drake TA, Lusis AJ."	8643601	5 months	female		"B, C57CL/6J; H, C3H/HeJ"				H	H	B	B	B	B	B	H		B	B
The prevalence of DCC in BXH strains and the correspondence of this phenotype with the parental genotype for microsatellite markers typed on proximal chromosome 7	D7Mit224	A locus on chromosome 7 determines myocardial cell necrosis and calcification (dystrophic cardiac calcinosis) in mice.	"Dystrophic cardiac calcinosis, an age-related cardiomyopathy that occurs among certain inbred strains of mice, involves myocardial injury, necrosis, and calcification. Using a complete linkage map approach and quantitative trait locus analysis, we sought to identify genetic loci determining dystrophic cardiac calcinosis in an F2 intercross of resistant C57BL/6J and susceptible C3H/HeJ inbred strains. We identified a single major locus, designated Dyscalc, located on proximal chromosome 7 in a region syntenic with human chromosomes 19q13 and 11p15. The statistical significance of Dyscalc (logarithm of odds score 14.6) was tested by analysis of permuted trait data. Analysis of BxH recombinant inbred strains confirmed the mapping position. The inheritance pattern indicated that this locus influences susceptibility of cells both to enter necrosis and to subsequently undergo calcification."	Proc Natl Acad Sci U S A 	1996	May	"Ivandic BT, Qiao JH, Machleder D, Liao F, Drake TA, Lusis AJ."	8643601	5 months	female		"B, C57CL/6J; H, C3H/HeJ"				H	H	B	B	B	B	H	H		H	H
The prevalence of DCC in BXH strains and the correspondence of this phenotype with the parental genotype for microsatellite markers typed on proximal chromosome 7	"D7Mit247, D7Mit25"	A locus on chromosome 7 determines myocardial cell necrosis and calcification (dystrophic cardiac calcinosis) in mice.	"Dystrophic cardiac calcinosis, an age-related cardiomyopathy that occurs among certain inbred strains of mice, involves myocardial injury, necrosis, and calcification. Using a complete linkage map approach and quantitative trait locus analysis, we sought to identify genetic loci determining dystrophic cardiac calcinosis in an F2 intercross of resistant C57BL/6J and susceptible C3H/HeJ inbred strains. We identified a single major locus, designated Dyscalc, located on proximal chromosome 7 in a region syntenic with human chromosomes 19q13 and 11p15. The statistical significance of Dyscalc (logarithm of odds score 14.6) was tested by analysis of permuted trait data. Analysis of BxH recombinant inbred strains confirmed the mapping position. The inheritance pattern indicated that this locus influences susceptibility of cells both to enter necrosis and to subsequently undergo calcification."	Proc Natl Acad Sci U S A 	1996	May	"Ivandic BT, Qiao JH, Machleder D, Liao F, Drake TA, Lusis AJ."	8643601	5 months	female		"B, C57CL/6J; H, C3H/HeJ"				H	H	H	H	B	B	H	H		H	H
The prevalence of DCC in BXH strains and the correspondence of this phenotype with the parental genotype for microsatellite markers typed on proximal chromosome 7	D7Mit227	A locus on chromosome 7 determines myocardial cell necrosis and calcification (dystrophic cardiac calcinosis) in mice.	"Dystrophic cardiac calcinosis, an age-related cardiomyopathy that occurs among certain inbred strains of mice, involves myocardial injury, necrosis, and calcification. Using a complete linkage map approach and quantitative trait locus analysis, we sought to identify genetic loci determining dystrophic cardiac calcinosis in an F2 intercross of resistant C57BL/6J and susceptible C3H/HeJ inbred strains. We identified a single major locus, designated Dyscalc, located on proximal chromosome 7 in a region syntenic with human chromosomes 19q13 and 11p15. The statistical significance of Dyscalc (logarithm of odds score 14.6) was tested by analysis of permuted trait data. Analysis of BxH recombinant inbred strains confirmed the mapping position. The inheritance pattern indicated that this locus influences susceptibility of cells both to enter necrosis and to subsequently undergo calcification."	Proc Natl Acad Sci U S A 	1996	May	"Ivandic BT, Qiao JH, Machleder D, Liao F, Drake TA, Lusis AJ."	8643601	5 months	female		"B, C57CL/6J; H, C3H/HeJ"				H	H	H	H	B	B	H	H		H	H
The prevalence of DCC in BXH strains and the correspondence of this phenotype with the parental genotype for microsatellite markers typed on proximal chromosome 7	D7Mit270	A locus on chromosome 7 determines myocardial cell necrosis and calcification (dystrophic cardiac calcinosis) in mice.	"Dystrophic cardiac calcinosis, an age-related cardiomyopathy that occurs among certain inbred strains of mice, involves myocardial injury, necrosis, and calcification. Using a complete linkage map approach and quantitative trait locus analysis, we sought to identify genetic loci determining dystrophic cardiac calcinosis in an F2 intercross of resistant C57BL/6J and susceptible C3H/HeJ inbred strains. We identified a single major locus, designated Dyscalc, located on proximal chromosome 7 in a region syntenic with human chromosomes 19q13 and 11p15. The statistical significance of Dyscalc (logarithm of odds score 14.6) was tested by analysis of permuted trait data. Analysis of BxH recombinant inbred strains confirmed the mapping position. The inheritance pattern indicated that this locus influences susceptibility of cells both to enter necrosis and to subsequently undergo calcification."	Proc Natl Acad Sci U S A 	1996	May	"Ivandic BT, Qiao JH, Machleder D, Liao F, Drake TA, Lusis AJ."	8643601	5 months	female		"B, C57CL/6J; H, C3H/HeJ"				H	H	H	B	B	B	H	H		H	H
The prevalence of DCC in BXH strains and the correspondence of this phenotype with the parental genotype for microsatellite markers typed on proximal chromosome 7	D7Mit229	A locus on chromosome 7 determines myocardial cell necrosis and calcification (dystrophic cardiac calcinosis) in mice.	"Dystrophic cardiac calcinosis, an age-related cardiomyopathy that occurs among certain inbred strains of mice, involves myocardial injury, necrosis, and calcification. Using a complete linkage map approach and quantitative trait locus analysis, we sought to identify genetic loci determining dystrophic cardiac calcinosis in an F2 intercross of resistant C57BL/6J and susceptible C3H/HeJ inbred strains. We identified a single major locus, designated Dyscalc, located on proximal chromosome 7 in a region syntenic with human chromosomes 19q13 and 11p15. The statistical significance of Dyscalc (logarithm of odds score 14.6) was tested by analysis of permuted trait data. Analysis of BxH recombinant inbred strains confirmed the mapping position. The inheritance pattern indicated that this locus influences susceptibility of cells both to enter necrosis and to subsequently undergo calcification."	Proc Natl Acad Sci U S A 	1996	May	"Ivandic BT, Qiao JH, Machleder D, Liao F, Drake TA, Lusis AJ."	8643601	5 months	female		"B, C57CL/6J; H, C3H/HeJ"				H	H	H	B	B	B	H	H		H	H
The prevalence of DCC in BXH strains and the correspondence of this phenotype with the parental genotype for microsatellite markers typed on proximal chromosome 7	D7Mit82	A locus on chromosome 7 determines myocardial cell necrosis and calcification (dystrophic cardiac calcinosis) in mice.	"Dystrophic cardiac calcinosis, an age-related cardiomyopathy that occurs among certain inbred strains of mice, involves myocardial injury, necrosis, and calcification. Using a complete linkage map approach and quantitative trait locus analysis, we sought to identify genetic loci determining dystrophic cardiac calcinosis in an F2 intercross of resistant C57BL/6J and susceptible C3H/HeJ inbred strains. We identified a single major locus, designated Dyscalc, located on proximal chromosome 7 in a region syntenic with human chromosomes 19q13 and 11p15. The statistical significance of Dyscalc (logarithm of odds score 14.6) was tested by analysis of permuted trait data. Analysis of BxH recombinant inbred strains confirmed the mapping position. The inheritance pattern indicated that this locus influences susceptibility of cells both to enter necrosis and to subsequently undergo calcification."	Proc Natl Acad Sci U S A 	1996	May	"Ivandic BT, Qiao JH, Machleder D, Liao F, Drake TA, Lusis AJ."	8643601	5 months	female		"B, C57CL/6J; H, C3H/HeJ"				H	H	H	B	H	B	H	H		H	H
The prevalence of DCC in BXH strains and the correspondence of this phenotype with the parental genotype for microsatellite markers typed on proximal chromosome 7	Prevalence of DCC	A locus on chromosome 7 determines myocardial cell necrosis and calcification (dystrophic cardiac calcinosis) in mice.	"Dystrophic cardiac calcinosis, an age-related cardiomyopathy that occurs among certain inbred strains of mice, involves myocardial injury, necrosis, and calcification. Using a complete linkage map approach and quantitative trait locus analysis, we sought to identify genetic loci determining dystrophic cardiac calcinosis in an F2 intercross of resistant C57BL/6J and susceptible C3H/HeJ inbred strains. We identified a single major locus, designated Dyscalc, located on proximal chromosome 7 in a region syntenic with human chromosomes 19q13 and 11p15. The statistical significance of Dyscalc (logarithm of odds score 14.6) was tested by analysis of permuted trait data. Analysis of BxH recombinant inbred strains confirmed the mapping position. The inheritance pattern indicated that this locus influences susceptibility of cells both to enter necrosis and to subsequently undergo calcification."	Proc Natl Acad Sci U S A 	1996	May	"Ivandic BT, Qiao JH, Machleder D, Liao F, Drake TA, Lusis AJ."	8643601	5 months	female		%				50	75	25	0	0	0	0	100		29	17
The prevalence of DCC in BXH strains and the correspondence of this phenotype with the parental genotype for microsatellite markers typed on proximal chromosome 7	Mice with DCC/ total	A locus on chromosome 7 determines myocardial cell necrosis and calcification (dystrophic cardiac calcinosis) in mice.	"Dystrophic cardiac calcinosis, an age-related cardiomyopathy that occurs among certain inbred strains of mice, involves myocardial injury, necrosis, and calcification. Using a complete linkage map approach and quantitative trait locus analysis, we sought to identify genetic loci determining dystrophic cardiac calcinosis in an F2 intercross of resistant C57BL/6J and susceptible C3H/HeJ inbred strains. We identified a single major locus, designated Dyscalc, located on proximal chromosome 7 in a region syntenic with human chromosomes 19q13 and 11p15. The statistical significance of Dyscalc (logarithm of odds score 14.6) was tested by analysis of permuted trait data. Analysis of BxH recombinant inbred strains confirmed the mapping position. The inheritance pattern indicated that this locus influences susceptibility of cells both to enter necrosis and to subsequently undergo calcification."	Proc Natl Acad Sci U S A 	1996	May	"Ivandic BT, Qiao JH, Machleder D, Liao F, Drake TA, Lusis AJ."	8643601	5 months	female		"B, C57CL/6J; H, C3H/HeJ"				8-Apr	8-Jun	4-Jan	0/ 8	0/ 3	0/ 7	0/ 5	9-Sep		7-Feb	7-Jan
Number of lavageable polymorphonuclear leukocytes in bronchoalveolar lavage returns from BXH RI strains 6 hours after :	acute (3h) exposure to 2 ppm ozone	Susceptibility to ozone-induced inflammation. I. Genetic control of the response to subacute exposure.	"We demonstrated previously that C57BL/6J (B6) inbred mice are susceptible and C3H/HeJ (C3) mice are resistant to airway inflammation that is induced by acute (3 h) exposure to 2 parts per million (ppm) ozone (O3). In the present study we tested the hypothesis that B6 and C3 mice are also differentially susceptible to the airway inflammatory responses to subacute (72 h) exposure to environmentally relevant concentrations of O3 (0.12 and 0.30 ppm). Male mice (20-25 g, 5-7 wk) were exposed continuously to 0.12 ppm O3, 0.30 ppm O3, or filtered air (control). Pulmonary inflammation was assessed after 24, 48, and 72 h by differential cell count and total protein in bronchoalveolar lavage (BAL) returns. Exposure to 0.12 ppm O3 caused significant influx of alveolar macrophages, polymorphonuclear leukocytes (PMNs), lymphocytes, and total BAL protein in both strains, but no differences in the magnitude of the responses were found between B6 and C3 mice. In contrast to the effect of 0.12 ppm O3, exposure to 0.30 ppm O3 elicited significantly greater numbers of inflammatory cells and BAL protein concentration in B6 mice relative to C3 mice. The phenotypes of the B6 and C3 mice were termed susceptible and resistant, respectively. To further evaluate the potential genetic contribution to the inflammatory response to 0.30 ppm O3, the F1, F2, and backcross progeny from B6 and C3 progenitors were examined. The ratios of susceptible and resistant phenotypes of these progeny support the hypothesis that a single autosomal recessive gene confers susceptibility to subacute O3-induced inflammation.(ABSTRACT TRUNCATED AT 250 WORDS)"	Am J Physiol	1993	Jan	"Kleeberger SR, Levitt RC, Zhang LY."	8430812	6 - 8 weeks	both		Number of PMNs in BAL (x10^3)	10	2	26	3	1	18		20	1	1		7	15	1
Number of lavageable polymorphonuclear leukocytes in bronchoalveolar lavage returns from BXH RI strains 6 hours after :	subacute (48h) exposure to 0.30 ppm ozone	Susceptibility to ozone-induced inflammation. I. Genetic control of the response to subacute exposure.	"We demonstrated previously that C57BL/6J (B6) inbred mice are susceptible and C3H/HeJ (C3) mice are resistant to airway inflammation that is induced by acute (3 h) exposure to 2 parts per million (ppm) ozone (O3). In the present study we tested the hypothesis that B6 and C3 mice are also differentially susceptible to the airway inflammatory responses to subacute (72 h) exposure to environmentally relevant concentrations of O3 (0.12 and 0.30 ppm). Male mice (20-25 g, 5-7 wk) were exposed continuously to 0.12 ppm O3, 0.30 ppm O3, or filtered air (control). Pulmonary inflammation was assessed after 24, 48, and 72 h by differential cell count and total protein in bronchoalveolar lavage (BAL) returns. Exposure to 0.12 ppm O3 caused significant influx of alveolar macrophages, polymorphonuclear leukocytes (PMNs), lymphocytes, and total BAL protein in both strains, but no differences in the magnitude of the responses were found between B6 and C3 mice. In contrast to the effect of 0.12 ppm O3, exposure to 0.30 ppm O3 elicited significantly greater numbers of inflammatory cells and BAL protein concentration in B6 mice relative to C3 mice. The phenotypes of the B6 and C3 mice were termed susceptible and resistant, respectively. To further evaluate the potential genetic contribution to the inflammatory response to 0.30 ppm O3, the F1, F2, and backcross progeny from B6 and C3 progenitors were examined. The ratios of susceptible and resistant phenotypes of these progeny support the hypothesis that a single autosomal recessive gene confers susceptibility to subacute O3-induced inflammation.(ABSTRACT TRUNCATED AT 250 WORDS)"	Am J Physiol	1993	Jan	"Kleeberger SR, Levitt RC, Zhang LY."	8430812	6 - 8 weeks	both		Number of PMNs in BAL (x10^3)	10	2	3	15	2	2		13	1	3		2	11	1
Phenotypes and Genotypes of Parental (C57BL/6J and C3H/HeJ) and of BXH RI Strains	Lesion scores	"Genetic evidence for a common pathway mediating oxidative stress, inflammatory gene induction, and aortic fatty streak formation in mice."	"In a previous survey of inbred mouse strains on an atherogenic diet, we observed that the susceptibility to aortic atherosclerotic lesion formation was associated with the accumulation of lipid peroxidation products, induction of inflammatory genes, and the activation of NF-kB-like transcription factors (Liao, F., A. Andalibi, F. C. deBeer, A. M. Fogelman, and A.J. Lusis. 1993. J. Clin. Invest. 91:2572-2579). We hypothesized that the inflammation-related processes were stimulated by oxidized lipids, since injection of minimally oxidized LDL (MM-LDL) activated the same set of genes. We now report that the induction of inflammatory genes and activation of NF-kB-like transcription factors cosegregate with aortic atherosclerotic lesion formation in BXH recombinant inbred strains derived from parental C57BL/6J (susceptible) and C3H/HeJ (resistant) mice. In addition, the accumulation of hepatic conjugated dienes exhibited a significant correlation with inflammatory gene activation. These results provide strong evidence for the role of inflammatory mediators inducible by oxidative stress in atherogenesis. They also suggest that a major gene contributing to aortic lesion development in this mouse model, designated Ath-1, may control either the accumulation of lipid peroxides in tissues or the cellular responses to such lipid peroxides."	J Clin Invest	1994	Aug	"Liao F, Andalibi A, Qiao JH, Allayee H, Fogelman AM, Lusis AJ."	8040344	4 - 6 months	female	3 - 9 animals	mm^3/section	"13,749"	673		"2,496"	473	563	665	"24,365"	250	"1,831"	"7,374"		"3,406"	"13,080"
Phenotypes and Genotypes of Parental (C57BL/6J and C3H/HeJ) and of BXH RI Strains	SAA units	"Genetic evidence for a common pathway mediating oxidative stress, inflammatory gene induction, and aortic fatty streak formation in mice."	"In a previous survey of inbred mouse strains on an atherogenic diet, we observed that the susceptibility to aortic atherosclerotic lesion formation was associated with the accumulation of lipid peroxidation products, induction of inflammatory genes, and the activation of NF-kB-like transcription factors (Liao, F., A. Andalibi, F. C. deBeer, A. M. Fogelman, and A.J. Lusis. 1993. J. Clin. Invest. 91:2572-2579). We hypothesized that the inflammation-related processes were stimulated by oxidized lipids, since injection of minimally oxidized LDL (MM-LDL) activated the same set of genes. We now report that the induction of inflammatory genes and activation of NF-kB-like transcription factors cosegregate with aortic atherosclerotic lesion formation in BXH recombinant inbred strains derived from parental C57BL/6J (susceptible) and C3H/HeJ (resistant) mice. In addition, the accumulation of hepatic conjugated dienes exhibited a significant correlation with inflammatory gene activation. These results provide strong evidence for the role of inflammatory mediators inducible by oxidative stress in atherogenesis. They also suggest that a major gene contributing to aortic lesion development in this mouse model, designated Ath-1, may control either the accumulation of lipid peroxides in tissues or the cellular responses to such lipid peroxides."	J Clin Invest	1994	Aug	"Liao F, Andalibi A, Qiao JH, Allayee H, Fogelman AM, Lusis AJ."	8040344	4 - 6 months	female	3 - 9 animals	Densitometric units of particular mRNAs normalized to those of 18S rRNA mRNA	15.7	3.4		6	5.3	5.4	3	8.5	1.9	3.8	12		5.5	7.4
Phenotypes and Genotypes of Parental (C57BL/6J and C3H/HeJ) and of BXH RI Strains	HO units	"Genetic evidence for a common pathway mediating oxidative stress, inflammatory gene induction, and aortic fatty streak formation in mice."	"In a previous survey of inbred mouse strains on an atherogenic diet, we observed that the susceptibility to aortic atherosclerotic lesion formation was associated with the accumulation of lipid peroxidation products, induction of inflammatory genes, and the activation of NF-kB-like transcription factors (Liao, F., A. Andalibi, F. C. deBeer, A. M. Fogelman, and A.J. Lusis. 1993. J. Clin. Invest. 91:2572-2579). We hypothesized that the inflammation-related processes were stimulated by oxidized lipids, since injection of minimally oxidized LDL (MM-LDL) activated the same set of genes. We now report that the induction of inflammatory genes and activation of NF-kB-like transcription factors cosegregate with aortic atherosclerotic lesion formation in BXH recombinant inbred strains derived from parental C57BL/6J (susceptible) and C3H/HeJ (resistant) mice. In addition, the accumulation of hepatic conjugated dienes exhibited a significant correlation with inflammatory gene activation. These results provide strong evidence for the role of inflammatory mediators inducible by oxidative stress in atherogenesis. They also suggest that a major gene contributing to aortic lesion development in this mouse model, designated Ath-1, may control either the accumulation of lipid peroxides in tissues or the cellular responses to such lipid peroxides."	J Clin Invest	1994	Aug	"Liao F, Andalibi A, Qiao JH, Allayee H, Fogelman AM, Lusis AJ."	8040344	4 - 6 months	female	3 - 9 animals	Densitometric units of particular mRNAs normalized to those of 18S rRNA mRNA	3.2	1.5		2	0.9	3	1.5	5.3	0.4	2.2	5.9		1.1	1.4
Phenotypes and Genotypes of Parental (C57BL/6J and C3H/HeJ) and of BXH RI Strains	apo A-IV units	"Genetic evidence for a common pathway mediating oxidative stress, inflammatory gene induction, and aortic fatty streak formation in mice."	"In a previous survey of inbred mouse strains on an atherogenic diet, we observed that the susceptibility to aortic atherosclerotic lesion formation was associated with the accumulation of lipid peroxidation products, induction of inflammatory genes, and the activation of NF-kB-like transcription factors (Liao, F., A. Andalibi, F. C. deBeer, A. M. Fogelman, and A.J. Lusis. 1993. J. Clin. Invest. 91:2572-2579). We hypothesized that the inflammation-related processes were stimulated by oxidized lipids, since injection of minimally oxidized LDL (MM-LDL) activated the same set of genes. We now report that the induction of inflammatory genes and activation of NF-kB-like transcription factors cosegregate with aortic atherosclerotic lesion formation in BXH recombinant inbred strains derived from parental C57BL/6J (susceptible) and C3H/HeJ (resistant) mice. In addition, the accumulation of hepatic conjugated dienes exhibited a significant correlation with inflammatory gene activation. These results provide strong evidence for the role of inflammatory mediators inducible by oxidative stress in atherogenesis. They also suggest that a major gene contributing to aortic lesion development in this mouse model, designated Ath-1, may control either the accumulation of lipid peroxides in tissues or the cellular responses to such lipid peroxides."	J Clin Invest	1994	Aug	"Liao F, Andalibi A, Qiao JH, Allayee H, Fogelman AM, Lusis AJ."	8040344	4 - 6 months	female	3 - 9 animals	Densitometric units of particular mRNAs normalized to those of 18S rRNA mRNA				2.7	3.8	7.8	5	7	5.8	4.2	3.9		4	3.9
Phenotypes and Genotypes of Parental (C57BL/6J and C3H/HeJ) and of BXH RI Strains	Nf-kB-like	"Genetic evidence for a common pathway mediating oxidative stress, inflammatory gene induction, and aortic fatty streak formation in mice."	"In a previous survey of inbred mouse strains on an atherogenic diet, we observed that the susceptibility to aortic atherosclerotic lesion formation was associated with the accumulation of lipid peroxidation products, induction of inflammatory genes, and the activation of NF-kB-like transcription factors (Liao, F., A. Andalibi, F. C. deBeer, A. M. Fogelman, and A.J. Lusis. 1993. J. Clin. Invest. 91:2572-2579). We hypothesized that the inflammation-related processes were stimulated by oxidized lipids, since injection of minimally oxidized LDL (MM-LDL) activated the same set of genes. We now report that the induction of inflammatory genes and activation of NF-kB-like transcription factors cosegregate with aortic atherosclerotic lesion formation in BXH recombinant inbred strains derived from parental C57BL/6J (susceptible) and C3H/HeJ (resistant) mice. In addition, the accumulation of hepatic conjugated dienes exhibited a significant correlation with inflammatory gene activation. These results provide strong evidence for the role of inflammatory mediators inducible by oxidative stress in atherogenesis. They also suggest that a major gene contributing to aortic lesion development in this mouse model, designated Ath-1, may control either the accumulation of lipid peroxides in tissues or the cellular responses to such lipid peroxides."	J Clin Invest	1994	Aug	"Liao F, Andalibi A, Qiao JH, Allayee H, Fogelman AM, Lusis AJ."	8040344	4 - 6 months	female	3 - 9 animals	Denitometric units of shifted radioactive-labeled olgonucleotide bands on mobility shift assays	840	20		126	47	23	232	786	20	59	1425		76	286
Phenotypes and Genotypes of Parental (C57BL/6J and C3H/HeJ) and of BXH RI Strains	Conjugated dienes	"Genetic evidence for a common pathway mediating oxidative stress, inflammatory gene induction, and aortic fatty streak formation in mice."	"In a previous survey of inbred mouse strains on an atherogenic diet, we observed that the susceptibility to aortic atherosclerotic lesion formation was associated with the accumulation of lipid peroxidation products, induction of inflammatory genes, and the activation of NF-kB-like transcription factors (Liao, F., A. Andalibi, F. C. deBeer, A. M. Fogelman, and A.J. Lusis. 1993. J. Clin. Invest. 91:2572-2579). We hypothesized that the inflammation-related processes were stimulated by oxidized lipids, since injection of minimally oxidized LDL (MM-LDL) activated the same set of genes. We now report that the induction of inflammatory genes and activation of NF-kB-like transcription factors cosegregate with aortic atherosclerotic lesion formation in BXH recombinant inbred strains derived from parental C57BL/6J (susceptible) and C3H/HeJ (resistant) mice. In addition, the accumulation of hepatic conjugated dienes exhibited a significant correlation with inflammatory gene activation. These results provide strong evidence for the role of inflammatory mediators inducible by oxidative stress in atherogenesis. They also suggest that a major gene contributing to aortic lesion development in this mouse model, designated Ath-1, may control either the accumulation of lipid peroxides in tissues or the cellular responses to such lipid peroxides."	J Clin Invest	1994	Aug	"Liao F, Andalibi A, Qiao JH, Allayee H, Fogelman AM, Lusis AJ."	8040344	4 - 6 months	female	3 - 9 animals	Conjugated dienes in the liver tissue (mmol/g net weight)	1250	564		1148	1166	1075	829	1431	682	680	1954		280	654
Phenotypes and Genotypes of Parental (C57BL/6J and C3H/HeJ) and of BXH RI Strains	Lps allele	"Genetic evidence for a common pathway mediating oxidative stress, inflammatory gene induction, and aortic fatty streak formation in mice."	"In a previous survey of inbred mouse strains on an atherogenic diet, we observed that the susceptibility to aortic atherosclerotic lesion formation was associated with the accumulation of lipid peroxidation products, induction of inflammatory genes, and the activation of NF-kB-like transcription factors (Liao, F., A. Andalibi, F. C. deBeer, A. M. Fogelman, and A.J. Lusis. 1993. J. Clin. Invest. 91:2572-2579). We hypothesized that the inflammation-related processes were stimulated by oxidized lipids, since injection of minimally oxidized LDL (MM-LDL) activated the same set of genes. We now report that the induction of inflammatory genes and activation of NF-kB-like transcription factors cosegregate with aortic atherosclerotic lesion formation in BXH recombinant inbred strains derived from parental C57BL/6J (susceptible) and C3H/HeJ (resistant) mice. In addition, the accumulation of hepatic conjugated dienes exhibited a significant correlation with inflammatory gene activation. These results provide strong evidence for the role of inflammatory mediators inducible by oxidative stress in atherogenesis. They also suggest that a major gene contributing to aortic lesion development in this mouse model, designated Ath-1, may control either the accumulation of lipid peroxides in tissues or the cellular responses to such lipid peroxides."	J Clin Invest	1994	Aug	"Liao F, Andalibi A, Qiao JH, Allayee H, Fogelman AM, Lusis AJ."	8040344	4 - 6 months	female	3 - 9 animals	B = inherited from C57BL/6J; H = inherited from C3H/HeJ	B	H		H	H	H	H	H	H	B	B		B	B
SDP of MMTV proviral loci in the BXH RI strain set	"Mtv-1, 7"	Segregation patterns of endogenous mouse mammary tumor viruses in five recombinant inbred strain sets.	"We identified mouse mammary tumor proviral loci in the AKR/J, C3H/HeJ, C57BL/6J, C57L/J, DBA/2J, and SWR/J inbred mouse strains and determined their segregation patterns in the AKXD, AKXL, BXD, BXH, and SWXL recombinant inbred strain sets. Two new Mtv loci, Mtv-29 and Mtv-30, were identified. Mtv-30 was genetically mapped to chromosome 12. Additionally, two previously identified Mtv loci, Mtv-14 and Mtv-23, were genetically mapped to chromosome 4 and chromosome 6, respectively."	J Virol	1990	Sept	"Lee BK, Eicher EM."	2166832				B = C57BL/6J; H =C3H/HeJ			H	H	H	H	B	H	B	H	H	H	H	H
SDP of MMTV proviral loci in the BXH RI strain set	"Mtv6, 16"	Segregation patterns of endogenous mouse mammary tumor viruses in five recombinant inbred strain sets.	"We identified mouse mammary tumor proviral loci in the AKR/J, C3H/HeJ, C57BL/6J, C57L/J, DBA/2J, and SWR/J inbred mouse strains and determined their segregation patterns in the AKXD, AKXL, BXD, BXH, and SWXL recombinant inbred strain sets. Two new Mtv loci, Mtv-29 and Mtv-30, were identified. Mtv-30 was genetically mapped to chromosome 12. Additionally, two previously identified Mtv loci, Mtv-14 and Mtv-23, were genetically mapped to chromosome 4 and chromosome 6, respectively."	J Virol	1990	Sept	"Lee BK, Eicher EM."	2166832				B = C57BL/6J; H =C3H/HeJ			B	B	H	H	B	H	B	B	H	H	B	H
SDP of MMTV proviral loci in the BXH RI strain set	"Mtv9, 12"	Segregation patterns of endogenous mouse mammary tumor viruses in five recombinant inbred strain sets.	"We identified mouse mammary tumor proviral loci in the AKR/J, C3H/HeJ, C57BL/6J, C57L/J, DBA/2J, and SWR/J inbred mouse strains and determined their segregation patterns in the AKXD, AKXL, BXD, BXH, and SWXL recombinant inbred strain sets. Two new Mtv loci, Mtv-29 and Mtv-30, were identified. Mtv-30 was genetically mapped to chromosome 12. Additionally, two previously identified Mtv loci, Mtv-14 and Mtv-23, were genetically mapped to chromosome 4 and chromosome 6, respectively."	J Virol	1990	Sept	"Lee BK, Eicher EM."	2166832				B = C57BL/6J; H =C3H/HeJ			B	B	B	B	H	B	H	H	B	H	H	H
SDP of MMTV proviral loci in the BXH RI strain set	"Mtv11, 14"	Segregation patterns of endogenous mouse mammary tumor viruses in five recombinant inbred strain sets.	"We identified mouse mammary tumor proviral loci in the AKR/J, C3H/HeJ, C57BL/6J, C57L/J, DBA/2J, and SWR/J inbred mouse strains and determined their segregation patterns in the AKXD, AKXL, BXD, BXH, and SWXL recombinant inbred strain sets. Two new Mtv loci, Mtv-29 and Mtv-30, were identified. Mtv-30 was genetically mapped to chromosome 12. Additionally, two previously identified Mtv loci, Mtv-14 and Mtv-23, were genetically mapped to chromosome 4 and chromosome 6, respectively."	J Virol	1990	Sept	"Lee BK, Eicher EM."	2166832				B = C57BL/6J; H =C3H/HeJ			H	B	H	B	B	B	B	B	H	H	H	H
SDP of MMTV proviral loci in the BXH RI strain set	"Mtv14, 4"	Segregation patterns of endogenous mouse mammary tumor viruses in five recombinant inbred strain sets.	"We identified mouse mammary tumor proviral loci in the AKR/J, C3H/HeJ, C57BL/6J, C57L/J, DBA/2J, and SWR/J inbred mouse strains and determined their segregation patterns in the AKXD, AKXL, BXD, BXH, and SWXL recombinant inbred strain sets. Two new Mtv loci, Mtv-29 and Mtv-30, were identified. Mtv-30 was genetically mapped to chromosome 12. Additionally, two previously identified Mtv loci, Mtv-14 and Mtv-23, were genetically mapped to chromosome 4 and chromosome 6, respectively."	J Virol	1990	Sept	"Lee BK, Eicher EM."	2166832				B = C57BL/6J; H =C3H/HeJ			B	B	B	H	H	H	B	B	H	H	B	B
SDP of MMTV proviral loci in the BXH RI strain set	"Mtv17, 4"	Segregation patterns of endogenous mouse mammary tumor viruses in five recombinant inbred strain sets.	"We identified mouse mammary tumor proviral loci in the AKR/J, C3H/HeJ, C57BL/6J, C57L/J, DBA/2J, and SWR/J inbred mouse strains and determined their segregation patterns in the AKXD, AKXL, BXD, BXH, and SWXL recombinant inbred strain sets. Two new Mtv loci, Mtv-29 and Mtv-30, were identified. Mtv-30 was genetically mapped to chromosome 12. Additionally, two previously identified Mtv loci, Mtv-14 and Mtv-23, were genetically mapped to chromosome 4 and chromosome 6, respectively."	J Virol	1990	Sept	"Lee BK, Eicher EM."	2166832				B = C57BL/6J; H =C3H/HeJ			B	H	B	H	H	H	B	H	B	H	H	B
"Inheritance of EcoRV apoB gene polymorphism, LDL size polymorphism, and other chromosome 12 markers"	LDL size	Genetic heterogeneity of plasma lipoproteins in the mouse: control of low density lipoprotein particle sizes by genetic factors.	"In order to assess the genetic control of sizes and concentrations of mouse plasma low density (LDL) and high density lipoproteins (HDL), we used gel permeation fast protein liquid chromatography (FPLC) and nondenaturing gradient polyacrylamide gel electrophoresis to measure the particle sizes of LDL and HDL. Using chromatography we also quantified LDL-cholesterol and HDL-cholesterol concentrations in plasma and used them as indexes of plasma concentrations of the respective particles among 10 inbred strains (AKR/J, BALB/cByJ, C3H/HeJ, C57BL/6J, C57BL/6ByJ, C57L/J, DBA/1LacJ, 129/J, NZB/BINJ, SWR/J) and three sets of recombinant inbred (RI) strains (AKXL/TyJ, BXH/TyJ, CXB/ByJ) of mice. HDL had a dichotomous distribution among the 10 inbred strains. One group had large HDL particle sizes and high HDL-cholesterol concentrations. Another group had smaller HDL particles and lower HDL-cholesterol concentrations, and HDL sizes and HDL-cholesterol concentrations were significantly correlated. In the RI strains, HDL sizes and HDL-cholesterol cholesterol concentrations clearly segregated with one or another of the progenitor strains, and RI strain distributions showed a strong linkage to the apolipoprotein (apo) A-II gene (Apoa-2). In contrast, LDL-cholesterol concentrations and particle sizes on FPLC did not show dichotomous distributions among the 10 inbred strains. In RI strains, the configuration of the LDL FPLC profiles and LDL-cholesterol concentrations did resemble one or another of the progenitors in the majority of cases, but LDLs of several RI strains resembled neither progenitor strain in profile configuration, and LDL-cholesterol concentrations were both greater and smaller than those of progenitor strains. However, LDL particle diameters (as judged by peaks of LDL-cholesterol profiles) did segregate with progenitors in 29/33 (88%) of RI strains suggesting that a major gene may affect LDL size. In attempting to identify a major LDL-size determining gene, we compared apoB gene restriction fragment length polymorphisms (RFLPs) to the distributions of peak LDL sizes in RI strains. Concordance rates of peak LDL sizes to apoB gene polymorphisms were 18/22 (82%) for the EcoRV RFLP, 5/7 (71%) for HindIII RFLP, and 23/29 (79%) for both (range of P values 0.90-0.95). Thus we could not unequivocally implicate the apoB gene in determining the size of LDL particles. In summary, the genetic control of LDL sizes is more complicated than is the case for HDL; however, the differences in LDL size among these strains of mice may be controlled by a major, as yet unidentified, gene."	 J Lipid Res	1990	Mar	"Jiao S, Cole TG, Kitchens RT, Pfleger B, Schonfeld G."	1971301	8 - 10 weeks	female		B = C57BL/6J; H =C3H/HeJ			B	B	H	H	H	B	H				H	B
"Inheritance of EcoRV apoB gene polymorphism, LDL size polymorphism, and other chromosome 12 markers"	Rnr - 12	Genetic heterogeneity of plasma lipoproteins in the mouse: control of low density lipoprotein particle sizes by genetic factors.	"In order to assess the genetic control of sizes and concentrations of mouse plasma low density (LDL) and high density lipoproteins (HDL), we used gel permeation fast protein liquid chromatography (FPLC) and nondenaturing gradient polyacrylamide gel electrophoresis to measure the particle sizes of LDL and HDL. Using chromatography we also quantified LDL-cholesterol and HDL-cholesterol concentrations in plasma and used them as indexes of plasma concentrations of the respective particles among 10 inbred strains (AKR/J, BALB/cByJ, C3H/HeJ, C57BL/6J, C57BL/6ByJ, C57L/J, DBA/1LacJ, 129/J, NZB/BINJ, SWR/J) and three sets of recombinant inbred (RI) strains (AKXL/TyJ, BXH/TyJ, CXB/ByJ) of mice. HDL had a dichotomous distribution among the 10 inbred strains. One group had large HDL particle sizes and high HDL-cholesterol concentrations. Another group had smaller HDL particles and lower HDL-cholesterol concentrations, and HDL sizes and HDL-cholesterol concentrations were significantly correlated. In the RI strains, HDL sizes and HDL-cholesterol cholesterol concentrations clearly segregated with one or another of the progenitor strains, and RI strain distributions showed a strong linkage to the apolipoprotein (apo) A-II gene (Apoa-2). In contrast, LDL-cholesterol concentrations and particle sizes on FPLC did not show dichotomous distributions among the 10 inbred strains. In RI strains, the configuration of the LDL FPLC profiles and LDL-cholesterol concentrations did resemble one or another of the progenitors in the majority of cases, but LDLs of several RI strains resembled neither progenitor strain in profile configuration, and LDL-cholesterol concentrations were both greater and smaller than those of progenitor strains. However, LDL particle diameters (as judged by peaks of LDL-cholesterol profiles) did segregate with progenitors in 29/33 (88%) of RI strains suggesting that a major gene may affect LDL size. In attempting to identify a major LDL-size determining gene, we compared apoB gene restriction fragment length polymorphisms (RFLPs) to the distributions of peak LDL sizes in RI strains. Concordance rates of peak LDL sizes to apoB gene polymorphisms were 18/22 (82%) for the EcoRV RFLP, 5/7 (71%) for HindIII RFLP, and 23/29 (79%) for both (range of P values 0.90-0.95). Thus we could not unequivocally implicate the apoB gene in determining the size of LDL particles. In summary, the genetic control of LDL sizes is more complicated than is the case for HDL; however, the differences in LDL size among these strains of mice may be controlled by a major, as yet unidentified, gene."	 J Lipid Res	1990	Mar	"Jiao S, Cole TG, Kitchens RT, Pfleger B, Schonfeld G."	1971301	8 - 10 weeks	female		B = C57BL/6J; H =C3H/HeJ			B	B	B	H	H	B	H				H	H
"Inheritance of EcoRV apoB gene polymorphism, LDL size polymorphism, and other chromosome 12 markers"	Apob	Genetic heterogeneity of plasma lipoproteins in the mouse: control of low density lipoprotein particle sizes by genetic factors.	"In order to assess the genetic control of sizes and concentrations of mouse plasma low density (LDL) and high density lipoproteins (HDL), we used gel permeation fast protein liquid chromatography (FPLC) and nondenaturing gradient polyacrylamide gel electrophoresis to measure the particle sizes of LDL and HDL. Using chromatography we also quantified LDL-cholesterol and HDL-cholesterol concentrations in plasma and used them as indexes of plasma concentrations of the respective particles among 10 inbred strains (AKR/J, BALB/cByJ, C3H/HeJ, C57BL/6J, C57BL/6ByJ, C57L/J, DBA/1LacJ, 129/J, NZB/BINJ, SWR/J) and three sets of recombinant inbred (RI) strains (AKXL/TyJ, BXH/TyJ, CXB/ByJ) of mice. HDL had a dichotomous distribution among the 10 inbred strains. One group had large HDL particle sizes and high HDL-cholesterol concentrations. Another group had smaller HDL particles and lower HDL-cholesterol concentrations, and HDL sizes and HDL-cholesterol concentrations were significantly correlated. In the RI strains, HDL sizes and HDL-cholesterol cholesterol concentrations clearly segregated with one or another of the progenitor strains, and RI strain distributions showed a strong linkage to the apolipoprotein (apo) A-II gene (Apoa-2). In contrast, LDL-cholesterol concentrations and particle sizes on FPLC did not show dichotomous distributions among the 10 inbred strains. In RI strains, the configuration of the LDL FPLC profiles and LDL-cholesterol concentrations did resemble one or another of the progenitors in the majority of cases, but LDLs of several RI strains resembled neither progenitor strain in profile configuration, and LDL-cholesterol concentrations were both greater and smaller than those of progenitor strains. However, LDL particle diameters (as judged by peaks of LDL-cholesterol profiles) did segregate with progenitors in 29/33 (88%) of RI strains suggesting that a major gene may affect LDL size. In attempting to identify a major LDL-size determining gene, we compared apoB gene restriction fragment length polymorphisms (RFLPs) to the distributions of peak LDL sizes in RI strains. Concordance rates of peak LDL sizes to apoB gene polymorphisms were 18/22 (82%) for the EcoRV RFLP, 5/7 (71%) for HindIII RFLP, and 23/29 (79%) for both (range of P values 0.90-0.95). Thus we could not unequivocally implicate the apoB gene in determining the size of LDL particles. In summary, the genetic control of LDL sizes is more complicated than is the case for HDL; however, the differences in LDL size among these strains of mice may be controlled by a major, as yet unidentified, gene."	 J Lipid Res	1990	Mar	"Jiao S, Cole TG, Kitchens RT, Pfleger B, Schonfeld G."	1971301	8 - 10 weeks	female		B = C57BL/6J; H =C3H/HeJ			B	B	B	H	H	B	H				H	H
"Inheritance of EcoRV apoB gene polymorphism, LDL size polymorphism, and other chromosome 12 markers"	D12 Nyu2	Genetic heterogeneity of plasma lipoproteins in the mouse: control of low density lipoprotein particle sizes by genetic factors.	"In order to assess the genetic control of sizes and concentrations of mouse plasma low density (LDL) and high density lipoproteins (HDL), we used gel permeation fast protein liquid chromatography (FPLC) and nondenaturing gradient polyacrylamide gel electrophoresis to measure the particle sizes of LDL and HDL. Using chromatography we also quantified LDL-cholesterol and HDL-cholesterol concentrations in plasma and used them as indexes of plasma concentrations of the respective particles among 10 inbred strains (AKR/J, BALB/cByJ, C3H/HeJ, C57BL/6J, C57BL/6ByJ, C57L/J, DBA/1LacJ, 129/J, NZB/BINJ, SWR/J) and three sets of recombinant inbred (RI) strains (AKXL/TyJ, BXH/TyJ, CXB/ByJ) of mice. HDL had a dichotomous distribution among the 10 inbred strains. One group had large HDL particle sizes and high HDL-cholesterol concentrations. Another group had smaller HDL particles and lower HDL-cholesterol concentrations, and HDL sizes and HDL-cholesterol concentrations were significantly correlated. In the RI strains, HDL sizes and HDL-cholesterol cholesterol concentrations clearly segregated with one or another of the progenitor strains, and RI strain distributions showed a strong linkage to the apolipoprotein (apo) A-II gene (Apoa-2). In contrast, LDL-cholesterol concentrations and particle sizes on FPLC did not show dichotomous distributions among the 10 inbred strains. In RI strains, the configuration of the LDL FPLC profiles and LDL-cholesterol concentrations did resemble one or another of the progenitors in the majority of cases, but LDLs of several RI strains resembled neither progenitor strain in profile configuration, and LDL-cholesterol concentrations were both greater and smaller than those of progenitor strains. However, LDL particle diameters (as judged by peaks of LDL-cholesterol profiles) did segregate with progenitors in 29/33 (88%) of RI strains suggesting that a major gene may affect LDL size. In attempting to identify a major LDL-size determining gene, we compared apoB gene restriction fragment length polymorphisms (RFLPs) to the distributions of peak LDL sizes in RI strains. Concordance rates of peak LDL sizes to apoB gene polymorphisms were 18/22 (82%) for the EcoRV RFLP, 5/7 (71%) for HindIII RFLP, and 23/29 (79%) for both (range of P values 0.90-0.95). Thus we could not unequivocally implicate the apoB gene in determining the size of LDL particles. In summary, the genetic control of LDL sizes is more complicated than is the case for HDL; however, the differences in LDL size among these strains of mice may be controlled by a major, as yet unidentified, gene."	 J Lipid Res	1990	Mar	"Jiao S, Cole TG, Kitchens RT, Pfleger B, Schonfeld G."	1971301	8 - 10 weeks	female		B = C57BL/6J; H =C3H/HeJ			B	B	B	H	H	B	H				H	H
"Inheritance of EcoRV apoB gene polymorphism, LDL size polymorphism, and other chromosome 12 markers"	Ly- 18	Genetic heterogeneity of plasma lipoproteins in the mouse: control of low density lipoprotein particle sizes by genetic factors.	"In order to assess the genetic control of sizes and concentrations of mouse plasma low density (LDL) and high density lipoproteins (HDL), we used gel permeation fast protein liquid chromatography (FPLC) and nondenaturing gradient polyacrylamide gel electrophoresis to measure the particle sizes of LDL and HDL. Using chromatography we also quantified LDL-cholesterol and HDL-cholesterol concentrations in plasma and used them as indexes of plasma concentrations of the respective particles among 10 inbred strains (AKR/J, BALB/cByJ, C3H/HeJ, C57BL/6J, C57BL/6ByJ, C57L/J, DBA/1LacJ, 129/J, NZB/BINJ, SWR/J) and three sets of recombinant inbred (RI) strains (AKXL/TyJ, BXH/TyJ, CXB/ByJ) of mice. HDL had a dichotomous distribution among the 10 inbred strains. One group had large HDL particle sizes and high HDL-cholesterol concentrations. Another group had smaller HDL particles and lower HDL-cholesterol concentrations, and HDL sizes and HDL-cholesterol concentrations were significantly correlated. In the RI strains, HDL sizes and HDL-cholesterol cholesterol concentrations clearly segregated with one or another of the progenitor strains, and RI strain distributions showed a strong linkage to the apolipoprotein (apo) A-II gene (Apoa-2). In contrast, LDL-cholesterol concentrations and particle sizes on FPLC did not show dichotomous distributions among the 10 inbred strains. In RI strains, the configuration of the LDL FPLC profiles and LDL-cholesterol concentrations did resemble one or another of the progenitors in the majority of cases, but LDLs of several RI strains resembled neither progenitor strain in profile configuration, and LDL-cholesterol concentrations were both greater and smaller than those of progenitor strains. However, LDL particle diameters (as judged by peaks of LDL-cholesterol profiles) did segregate with progenitors in 29/33 (88%) of RI strains suggesting that a major gene may affect LDL size. In attempting to identify a major LDL-size determining gene, we compared apoB gene restriction fragment length polymorphisms (RFLPs) to the distributions of peak LDL sizes in RI strains. Concordance rates of peak LDL sizes to apoB gene polymorphisms were 18/22 (82%) for the EcoRV RFLP, 5/7 (71%) for HindIII RFLP, and 23/29 (79%) for both (range of P values 0.90-0.95). Thus we could not unequivocally implicate the apoB gene in determining the size of LDL particles. In summary, the genetic control of LDL sizes is more complicated than is the case for HDL; however, the differences in LDL size among these strains of mice may be controlled by a major, as yet unidentified, gene."	 J Lipid Res	1990	Mar	"Jiao S, Cole TG, Kitchens RT, Pfleger B, Schonfeld G."	1971301	8 - 10 weeks	female		B = C57BL/6J; H =C3H/HeJ			B	B	B	B	H	B	H				H	H
Mitogenic and adjuvant responses to LPS in BXH recombinant inbred strains	Mitogenic Response: No LPS	The response of recombinant inbred strains of mice to bacterial lipopolysaccharides.	"Fourteen recombinant inbred strains of mice have been produced by the inbreeding of the F2 generation of a cross between C57BL/6J and C3H/HeJ progenitor mice. The responses of these BXH strains to bacterial lipopolysaccharides (LPS) have been characterized. Four BXH strains are high LPS responders and nine strains are low LPS responders. One BXH strain shows intermediate responsiveness which may reflect residual heterozygosity. F1 hybrid mice from low x high responder strains were intermediate in their response to LPS suggesting additive genetic control. The LPS responses in backcross mice from the F1 x low LPS responders showed segregation consistent with LPS responsiveness being determined by a single gene. In 13/14 BXH strains, there was concordant inheritance of LPS responsiveness and the major urinary protein locus Mup-1b. The association of the expression of the Mup-1 alleles with LPS responsiveness in the BXH strains suggests that the defective LPS response gene in C3H/HeJ mice is located on chromosome 4."	J Immunol	1977	June	"Watson J, Riblet R, Taylor BA."	325138	6 - 12 weeks	both		cpm x10^-3	4.7	4.4	1.1	1.1	3.7	3.3	2.2	1.2	3.7	3.3	2.2	2.8	3.9	3.5
Mitogenic and adjuvant responses to LPS in BXH recombinant inbred strains	Mitogenic Response:  5 micrograms	The response of recombinant inbred strains of mice to bacterial lipopolysaccharides.	"Fourteen recombinant inbred strains of mice have been produced by the inbreeding of the F2 generation of a cross between C57BL/6J and C3H/HeJ progenitor mice. The responses of these BXH strains to bacterial lipopolysaccharides (LPS) have been characterized. Four BXH strains are high LPS responders and nine strains are low LPS responders. One BXH strain shows intermediate responsiveness which may reflect residual heterozygosity. F1 hybrid mice from low x high responder strains were intermediate in their response to LPS suggesting additive genetic control. The LPS responses in backcross mice from the F1 x low LPS responders showed segregation consistent with LPS responsiveness being determined by a single gene. In 13/14 BXH strains, there was concordant inheritance of LPS responsiveness and the major urinary protein locus Mup-1b. The association of the expression of the Mup-1 alleles with LPS responsiveness in the BXH strains suggests that the defective LPS response gene in C3H/HeJ mice is located on chromosome 4."	J Immunol	1977	June	"Watson J, Riblet R, Taylor BA."	325138	6 - 12 weeks	both		cpm x10^-3	17.8	4.7	2.8	2.2	5.7	4.1	2.3	1.5	4	7.2	22	4.8	21.1	11.7
Mitogenic and adjuvant responses to LPS in BXH recombinant inbred strains	Mitogenic Response: 25 micrograms	The response of recombinant inbred strains of mice to bacterial lipopolysaccharides.	"Fourteen recombinant inbred strains of mice have been produced by the inbreeding of the F2 generation of a cross between C57BL/6J and C3H/HeJ progenitor mice. The responses of these BXH strains to bacterial lipopolysaccharides (LPS) have been characterized. Four BXH strains are high LPS responders and nine strains are low LPS responders. One BXH strain shows intermediate responsiveness which may reflect residual heterozygosity. F1 hybrid mice from low x high responder strains were intermediate in their response to LPS suggesting additive genetic control. The LPS responses in backcross mice from the F1 x low LPS responders showed segregation consistent with LPS responsiveness being determined by a single gene. In 13/14 BXH strains, there was concordant inheritance of LPS responsiveness and the major urinary protein locus Mup-1b. The association of the expression of the Mup-1 alleles with LPS responsiveness in the BXH strains suggests that the defective LPS response gene in C3H/HeJ mice is located on chromosome 4."	J Immunol	1977	June	"Watson J, Riblet R, Taylor BA."	325138	6 - 12 weeks	both		cpm x10^-3	51.5	5.6	5.1	3.1	8.3	4.5	3	2.5	5.3	8.1	43.1	5.6	46.6	44.5
Mitogenic and adjuvant responses to LPS in BXH recombinant inbred strains	Serum Titers	The response of recombinant inbred strains of mice to bacterial lipopolysaccharides.	"Fourteen recombinant inbred strains of mice have been produced by the inbreeding of the F2 generation of a cross between C57BL/6J and C3H/HeJ progenitor mice. The responses of these BXH strains to bacterial lipopolysaccharides (LPS) have been characterized. Four BXH strains are high LPS responders and nine strains are low LPS responders. One BXH strain shows intermediate responsiveness which may reflect residual heterozygosity. F1 hybrid mice from low x high responder strains were intermediate in their response to LPS suggesting additive genetic control. The LPS responses in backcross mice from the F1 x low LPS responders showed segregation consistent with LPS responsiveness being determined by a single gene. In 13/14 BXH strains, there was concordant inheritance of LPS responsiveness and the major urinary protein locus Mup-1b. The association of the expression of the Mup-1 alleles with LPS responsiveness in the BXH strains suggests that the defective LPS response gene in C3H/HeJ mice is located on chromosome 4."	J Immunol	1977	June	"Watson J, Riblet R, Taylor BA."	325138	6 - 12 weeks	both		"The first number represents the titer if the prebleed serum, and the second represents the titer 7 days after immunization.  the seurm are presented as a reciprocal of the endpoint dilution.  The initial dilution was always 1/10"	<10 / 10	<10 / 1280	<10/ 10	<10 / 20	20-Oct	<10 / 40	Oct-80	<10/ 10	<10/ 10	Oct-80	10/ 320	<10/ 10	10/ 1280	10/ 320
Mitogenic and adjuvant responses to LPS in BXH recombinant inbred strains	LPS Response 	The response of recombinant inbred strains of mice to bacterial lipopolysaccharides.	"Fourteen recombinant inbred strains of mice have been produced by the inbreeding of the F2 generation of a cross between C57BL/6J and C3H/HeJ progenitor mice. The responses of these BXH strains to bacterial lipopolysaccharides (LPS) have been characterized. Four BXH strains are high LPS responders and nine strains are low LPS responders. One BXH strain shows intermediate responsiveness which may reflect residual heterozygosity. F1 hybrid mice from low x high responder strains were intermediate in their response to LPS suggesting additive genetic control. The LPS responses in backcross mice from the F1 x low LPS responders showed segregation consistent with LPS responsiveness being determined by a single gene. In 13/14 BXH strains, there was concordant inheritance of LPS responsiveness and the major urinary protein locus Mup-1b. The association of the expression of the Mup-1 alleles with LPS responsiveness in the BXH strains suggests that the defective LPS response gene in C3H/HeJ mice is located on chromosome 4."	J Immunol	1977	June	"Watson J, Riblet R, Taylor BA."	325138	6 - 12 weeks	both		High/ Low	high	low	low	low	low	low	low	low	low	low	high	low	high	high
Mitogenic and adjuvant responses to LPS in BXH recombinant inbred strains	Generations Tested	The response of recombinant inbred strains of mice to bacterial lipopolysaccharides.	"Fourteen recombinant inbred strains of mice have been produced by the inbreeding of the F2 generation of a cross between C57BL/6J and C3H/HeJ progenitor mice. The responses of these BXH strains to bacterial lipopolysaccharides (LPS) have been characterized. Four BXH strains are high LPS responders and nine strains are low LPS responders. One BXH strain shows intermediate responsiveness which may reflect residual heterozygosity. F1 hybrid mice from low x high responder strains were intermediate in their response to LPS suggesting additive genetic control. The LPS responses in backcross mice from the F1 x low LPS responders showed segregation consistent with LPS responsiveness being determined by a single gene. In 13/14 BXH strains, there was concordant inheritance of LPS responsiveness and the major urinary protein locus Mup-1b. The association of the expression of the Mup-1 alleles with LPS responsiveness in the BXH strains suggests that the defective LPS response gene in C3H/HeJ mice is located on chromosome 4."	J Immunol	1977	June	"Watson J, Riblet R, Taylor BA."	325138	6 - 12 weeks	both					"F14, F23"	"F16, F23"	"F15, F20"	"F15, F22"	F15	"F12, F19"	"F14, F23, F26"	"F15, F19BC4F4, F19BC4F5"	"F15, F23, 28, F29"	F14	"F15, F22, F28"	"F15, F22, F28"
Mitogenic and adjuvant responses to LPS in BXH recombinant inbred strains	H - 2	The response of recombinant inbred strains of mice to bacterial lipopolysaccharides.	"Fourteen recombinant inbred strains of mice have been produced by the inbreeding of the F2 generation of a cross between C57BL/6J and C3H/HeJ progenitor mice. The responses of these BXH strains to bacterial lipopolysaccharides (LPS) have been characterized. Four BXH strains are high LPS responders and nine strains are low LPS responders. One BXH strain shows intermediate responsiveness which may reflect residual heterozygosity. F1 hybrid mice from low x high responder strains were intermediate in their response to LPS suggesting additive genetic control. The LPS responses in backcross mice from the F1 x low LPS responders showed segregation consistent with LPS responsiveness being determined by a single gene. In 13/14 BXH strains, there was concordant inheritance of LPS responsiveness and the major urinary protein locus Mup-1b. The association of the expression of the Mup-1 alleles with LPS responsiveness in the BXH strains suggests that the defective LPS response gene in C3H/HeJ mice is located on chromosome 4."	J Immunol	1977	June	"Watson J, Riblet R, Taylor BA."	325138	6 - 12 weeks	both					k	k	b	k	k	b	b	b	b	k	k	b
Mitogenic and adjuvant responses to LPS in BXH recombinant inbred strains	Ig - 1	The response of recombinant inbred strains of mice to bacterial lipopolysaccharides.	"Fourteen recombinant inbred strains of mice have been produced by the inbreeding of the F2 generation of a cross between C57BL/6J and C3H/HeJ progenitor mice. The responses of these BXH strains to bacterial lipopolysaccharides (LPS) have been characterized. Four BXH strains are high LPS responders and nine strains are low LPS responders. One BXH strain shows intermediate responsiveness which may reflect residual heterozygosity. F1 hybrid mice from low x high responder strains were intermediate in their response to LPS suggesting additive genetic control. The LPS responses in backcross mice from the F1 x low LPS responders showed segregation consistent with LPS responsiveness being determined by a single gene. In 13/14 BXH strains, there was concordant inheritance of LPS responsiveness and the major urinary protein locus Mup-1b. The association of the expression of the Mup-1 alleles with LPS responsiveness in the BXH strains suggests that the defective LPS response gene in C3H/HeJ mice is located on chromosome 4."	J Immunol	1977	June	"Watson J, Riblet R, Taylor BA."	325138	6 - 12 weeks	both					a	b	a	a	a	b	a	b	b	a	b	a
Mitogenic and adjuvant responses to LPS in BXH recombinant inbred strains	Mup - 1	The response of recombinant inbred strains of mice to bacterial lipopolysaccharides.	"Fourteen recombinant inbred strains of mice have been produced by the inbreeding of the F2 generation of a cross between C57BL/6J and C3H/HeJ progenitor mice. The responses of these BXH strains to bacterial lipopolysaccharides (LPS) have been characterized. Four BXH strains are high LPS responders and nine strains are low LPS responders. One BXH strain shows intermediate responsiveness which may reflect residual heterozygosity. F1 hybrid mice from low x high responder strains were intermediate in their response to LPS suggesting additive genetic control. The LPS responses in backcross mice from the F1 x low LPS responders showed segregation consistent with LPS responsiveness being determined by a single gene. In 13/14 BXH strains, there was concordant inheritance of LPS responsiveness and the major urinary protein locus Mup-1b. The association of the expression of the Mup-1 alleles with LPS responsiveness in the BXH strains suggests that the defective LPS response gene in C3H/HeJ mice is located on chromosome 4."	J Immunol	1977	June	"Watson J, Riblet R, Taylor BA."	325138	6 - 12 weeks	both					a	a	a	a	a	a	a	b	b	a	a	b
Mitogenic and adjuvant responses to LPS in BXH recombinant inbred strains	LPS (Responder/ Nonresponder)	The response of recombinant inbred strains of mice to bacterial lipopolysaccharides.	"Fourteen recombinant inbred strains of mice have been produced by the inbreeding of the F2 generation of a cross between C57BL/6J and C3H/HeJ progenitor mice. The responses of these BXH strains to bacterial lipopolysaccharides (LPS) have been characterized. Four BXH strains are high LPS responders and nine strains are low LPS responders. One BXH strain shows intermediate responsiveness which may reflect residual heterozygosity. F1 hybrid mice from low x high responder strains were intermediate in their response to LPS suggesting additive genetic control. The LPS responses in backcross mice from the F1 x low LPS responders showed segregation consistent with LPS responsiveness being determined by a single gene. In 13/14 BXH strains, there was concordant inheritance of LPS responsiveness and the major urinary protein locus Mup-1b. The association of the expression of the Mup-1 alleles with LPS responsiveness in the BXH strains suggests that the defective LPS response gene in C3H/HeJ mice is located on chromosome 4."	J Immunol	1977	June	"Watson J, Riblet R, Taylor BA."	325138	6 - 12 weeks	both		Responder/ nonresponder			NR	NR	NR	NR	NR	NR	NR	R	R	NR	NR	R
Phenotypes and Genotypes of Parental (C57BL/ 6J and C3H/ HeJ) and of BXH Ri strains	Lesion scores	"Genetic evidence for a common pathway mediating oxidative stress, inflammatory gene induction, and aortic fatty streak formation in mice."	"In a previous survey of inbred mouse strains on an atherogenic diet, we observed that the susceptibility to aortic atherosclerotic lesion formation was associated with the accumulation of lipid peroxidation products, induction of inflammatory genes, and the activation of NF-kB-like transcription factors (Liao, F., A. Andalibi, F. C. deBeer, A. M. Fogelman, and A.J. Lusis. 1993. J. Clin. Invest. 91:2572-2579). We hypothesized that the inflammation-related processes were stimulated by oxidized lipids, since injection of minimally oxidized LDL (MM-LDL) activated the same set of genes. We now report that the induction of inflammatory genes and activation of NF-kB-like transcription factors cosegregate with aortic atherosclerotic lesion formation in BXH recombinant inbred strains derived from parental C57BL/6J (susceptible) and C3H/HeJ (resistant) mice. In addition, the accumulation of hepatic conjugated dienes exhibited a significant correlation with inflammatory gene activation. These results provide strong evidence for the role of inflammatory mediators inducible by oxidative stress in atherogenesis. They also suggest that a major gene contributing to aortic lesion development in this mouse model, designated Ath-1, may control either the accumulation of lipid peroxides in tissues or the cellular responses to such lipid peroxides."	J Clin Invest	1994	Aug	"Liao F, Andalibi A, Qiao JH, Allayee H, Fogelman AM, Lusis AJ."	8040344	4 - 6 months	both		um^2/ section	"13,749"	673		"2,496"	473	563	665	"24,365"	250	"1,831"	"7,724"		"3,406"	"13,080"
Phenotypes and Genotypes of Parental (C57BL/ 6J and C3H/ HeJ) and of BXH Ri strains	SAA units	"Genetic evidence for a common pathway mediating oxidative stress, inflammatory gene induction, and aortic fatty streak formation in mice."	"In a previous survey of inbred mouse strains on an atherogenic diet, we observed that the susceptibility to aortic atherosclerotic lesion formation was associated with the accumulation of lipid peroxidation products, induction of inflammatory genes, and the activation of NF-kB-like transcription factors (Liao, F., A. Andalibi, F. C. deBeer, A. M. Fogelman, and A.J. Lusis. 1993. J. Clin. Invest. 91:2572-2579). We hypothesized that the inflammation-related processes were stimulated by oxidized lipids, since injection of minimally oxidized LDL (MM-LDL) activated the same set of genes. We now report that the induction of inflammatory genes and activation of NF-kB-like transcription factors cosegregate with aortic atherosclerotic lesion formation in BXH recombinant inbred strains derived from parental C57BL/6J (susceptible) and C3H/HeJ (resistant) mice. In addition, the accumulation of hepatic conjugated dienes exhibited a significant correlation with inflammatory gene activation. These results provide strong evidence for the role of inflammatory mediators inducible by oxidative stress in atherogenesis. They also suggest that a major gene contributing to aortic lesion development in this mouse model, designated Ath-1, may control either the accumulation of lipid peroxides in tissues or the cellular responses to such lipid peroxides."	J Clin Invest	1994	Aug	"Liao F, Andalibi A, Qiao JH, Allayee H, Fogelman AM, Lusis AJ."	8040344	4 - 6 months	both			15.7	3.4		6	5.3	5.4	3	8.5	1.9	3.8	12		5.5	7.4
Phenotypes and Genotypes of Parental (C57BL/ 6J and C3H/ HeJ) and of BXH Ri strains	HO units	"Genetic evidence for a common pathway mediating oxidative stress, inflammatory gene induction, and aortic fatty streak formation in mice."	"In a previous survey of inbred mouse strains on an atherogenic diet, we observed that the susceptibility to aortic atherosclerotic lesion formation was associated with the accumulation of lipid peroxidation products, induction of inflammatory genes, and the activation of NF-kB-like transcription factors (Liao, F., A. Andalibi, F. C. deBeer, A. M. Fogelman, and A.J. Lusis. 1993. J. Clin. Invest. 91:2572-2579). We hypothesized that the inflammation-related processes were stimulated by oxidized lipids, since injection of minimally oxidized LDL (MM-LDL) activated the same set of genes. We now report that the induction of inflammatory genes and activation of NF-kB-like transcription factors cosegregate with aortic atherosclerotic lesion formation in BXH recombinant inbred strains derived from parental C57BL/6J (susceptible) and C3H/HeJ (resistant) mice. In addition, the accumulation of hepatic conjugated dienes exhibited a significant correlation with inflammatory gene activation. These results provide strong evidence for the role of inflammatory mediators inducible by oxidative stress in atherogenesis. They also suggest that a major gene contributing to aortic lesion development in this mouse model, designated Ath-1, may control either the accumulation of lipid peroxides in tissues or the cellular responses to such lipid peroxides."	J Clin Invest	1994	Aug	"Liao F, Andalibi A, Qiao JH, Allayee H, Fogelman AM, Lusis AJ."	8040344	4 - 6 months	both			3.2	1.5		2	0.9	3	1.5	5.3	0.4	2.2	5.9		1.1	1.4
Phenotypes and Genotypes of Parental (C57BL/ 6J and C3H/ HeJ) and of BXH Ri strains	apo A- IV units	"Genetic evidence for a common pathway mediating oxidative stress, inflammatory gene induction, and aortic fatty streak formation in mice."	"In a previous survey of inbred mouse strains on an atherogenic diet, we observed that the susceptibility to aortic atherosclerotic lesion formation was associated with the accumulation of lipid peroxidation products, induction of inflammatory genes, and the activation of NF-kB-like transcription factors (Liao, F., A. Andalibi, F. C. deBeer, A. M. Fogelman, and A.J. Lusis. 1993. J. Clin. Invest. 91:2572-2579). We hypothesized that the inflammation-related processes were stimulated by oxidized lipids, since injection of minimally oxidized LDL (MM-LDL) activated the same set of genes. We now report that the induction of inflammatory genes and activation of NF-kB-like transcription factors cosegregate with aortic atherosclerotic lesion formation in BXH recombinant inbred strains derived from parental C57BL/6J (susceptible) and C3H/HeJ (resistant) mice. In addition, the accumulation of hepatic conjugated dienes exhibited a significant correlation with inflammatory gene activation. These results provide strong evidence for the role of inflammatory mediators inducible by oxidative stress in atherogenesis. They also suggest that a major gene contributing to aortic lesion development in this mouse model, designated Ath-1, may control either the accumulation of lipid peroxides in tissues or the cellular responses to such lipid peroxides."	J Clin Invest	1994	Aug	"Liao F, Andalibi A, Qiao JH, Allayee H, Fogelman AM, Lusis AJ."	8040344	4 - 6 months	both		ND = not determined	ND	ND		2.7	3.8	7.8	5	7	5.8	4.2	3.9		4	3.9
Phenotypes and Genotypes of Parental (C57BL/ 6J and C3H/ HeJ) and of BXH Ri strains	NF - kb - like	"Genetic evidence for a common pathway mediating oxidative stress, inflammatory gene induction, and aortic fatty streak formation in mice."	"In a previous survey of inbred mouse strains on an atherogenic diet, we observed that the susceptibility to aortic atherosclerotic lesion formation was associated with the accumulation of lipid peroxidation products, induction of inflammatory genes, and the activation of NF-kB-like transcription factors (Liao, F., A. Andalibi, F. C. deBeer, A. M. Fogelman, and A.J. Lusis. 1993. J. Clin. Invest. 91:2572-2579). We hypothesized that the inflammation-related processes were stimulated by oxidized lipids, since injection of minimally oxidized LDL (MM-LDL) activated the same set of genes. We now report that the induction of inflammatory genes and activation of NF-kB-like transcription factors cosegregate with aortic atherosclerotic lesion formation in BXH recombinant inbred strains derived from parental C57BL/6J (susceptible) and C3H/HeJ (resistant) mice. In addition, the accumulation of hepatic conjugated dienes exhibited a significant correlation with inflammatory gene activation. These results provide strong evidence for the role of inflammatory mediators inducible by oxidative stress in atherogenesis. They also suggest that a major gene contributing to aortic lesion development in this mouse model, designated Ath-1, may control either the accumulation of lipid peroxides in tissues or the cellular responses to such lipid peroxides."	J Clin Invest	1994	Aug	"Liao F, Andalibi A, Qiao JH, Allayee H, Fogelman AM, Lusis AJ."	8040344	4 - 6 months	both			840	20		126	47	23	232	786	20	59	1425		76	286
Phenotypes and Genotypes of Parental (C57BL/ 6J and C3H/ HeJ) and of BXH Ri strains	Conjugated dienes	"Genetic evidence for a common pathway mediating oxidative stress, inflammatory gene induction, and aortic fatty streak formation in mice."	"In a previous survey of inbred mouse strains on an atherogenic diet, we observed that the susceptibility to aortic atherosclerotic lesion formation was associated with the accumulation of lipid peroxidation products, induction of inflammatory genes, and the activation of NF-kB-like transcription factors (Liao, F., A. Andalibi, F. C. deBeer, A. M. Fogelman, and A.J. Lusis. 1993. J. Clin. Invest. 91:2572-2579). We hypothesized that the inflammation-related processes were stimulated by oxidized lipids, since injection of minimally oxidized LDL (MM-LDL) activated the same set of genes. We now report that the induction of inflammatory genes and activation of NF-kB-like transcription factors cosegregate with aortic atherosclerotic lesion formation in BXH recombinant inbred strains derived from parental C57BL/6J (susceptible) and C3H/HeJ (resistant) mice. In addition, the accumulation of hepatic conjugated dienes exhibited a significant correlation with inflammatory gene activation. These results provide strong evidence for the role of inflammatory mediators inducible by oxidative stress in atherogenesis. They also suggest that a major gene contributing to aortic lesion development in this mouse model, designated Ath-1, may control either the accumulation of lipid peroxides in tissues or the cellular responses to such lipid peroxides."	J Clin Invest	1994	Aug	"Liao F, Andalibi A, Qiao JH, Allayee H, Fogelman AM, Lusis AJ."	8040344	4 - 6 months	both		umol/ g wet weight	1250	564		1148	1166	1075	829	1431	682	680	1954		560	654
Phenotypes and Genotypes of Parental (C57BL/ 6J and C3H/ HeJ) and of BXH Ri strains	LPS allele	"Genetic evidence for a common pathway mediating oxidative stress, inflammatory gene induction, and aortic fatty streak formation in mice."	"In a previous survey of inbred mouse strains on an atherogenic diet, we observed that the susceptibility to aortic atherosclerotic lesion formation was associated with the accumulation of lipid peroxidation products, induction of inflammatory genes, and the activation of NF-kB-like transcription factors (Liao, F., A. Andalibi, F. C. deBeer, A. M. Fogelman, and A.J. Lusis. 1993. J. Clin. Invest. 91:2572-2579). We hypothesized that the inflammation-related processes were stimulated by oxidized lipids, since injection of minimally oxidized LDL (MM-LDL) activated the same set of genes. We now report that the induction of inflammatory genes and activation of NF-kB-like transcription factors cosegregate with aortic atherosclerotic lesion formation in BXH recombinant inbred strains derived from parental C57BL/6J (susceptible) and C3H/HeJ (resistant) mice. In addition, the accumulation of hepatic conjugated dienes exhibited a significant correlation with inflammatory gene activation. These results provide strong evidence for the role of inflammatory mediators inducible by oxidative stress in atherogenesis. They also suggest that a major gene contributing to aortic lesion development in this mouse model, designated Ath-1, may control either the accumulation of lipid peroxides in tissues or the cellular responses to such lipid peroxides."	J Clin Invest	1994	Aug	"Liao F, Andalibi A, Qiao JH, Allayee H, Fogelman AM, Lusis AJ."	8040344	4 - 6 months	both		B = C57BL/6J; H =C3H/HeJ	B	H		H	H	H	H	H	H	B	B		B	B
"Inheritance of EcoRV apoB gene polymorphism, LDL size polymorphism, and other chromosome 12 markers"	LDL size	Genetic heterogeneity of plasma lipoproteins in the mouse: control of low density lipoprotein particle sizes by genetic factors.	"In order to assess the genetic control of sizes and concentrations of mouse plasma low density (LDL) and high density lipoproteins (HDL), we used gel permeation fast protein liquid chromatography (FPLC) and nondenaturing gradient polyacrylamide gel electrophoresis to measure the particle sizes of LDL and HDL. Using chromatography we also quantified LDL-cholesterol and HDL-cholesterol concentrations in plasma and used them as indexes of plasma concentrations of the respective particles among 10 inbred strains (AKR/J, BALB/cByJ, C3H/HeJ, C57BL/6J, C57BL/6ByJ, C57L/J, DBA/1LacJ, 129/J, NZB/BINJ, SWR/J) and three sets of recombinant inbred (RI) strains (AKXL/TyJ, BXH/TyJ, CXB/ByJ) of mice. HDL had a dichotomous distribution among the 10 inbred strains. One group had large HDL particle sizes and high HDL-cholesterol concentrations. Another group had smaller HDL particles and lower HDL-cholesterol concentrations, and HDL sizes and HDL-cholesterol concentrations were significantly correlated. In the RI strains, HDL sizes and HDL-cholesterol cholesterol concentrations clearly segregated with one or another of the progenitor strains, and RI strain distributions showed a strong linkage to the apolipoprotein (apo) A-II gene (Apoa-2). In contrast, LDL-cholesterol concentrations and particle sizes on FPLC did not show dichotomous distributions among the 10 inbred strains. In RI strains, the configuration of the LDL FPLC profiles and LDL-cholesterol concentrations did resemble one or another of the progenitors in the majority of cases, but LDLs of several RI strains resembled neither progenitor strain in profile configuration, and LDL-cholesterol concentrations were both greater and smaller than those of progenitor strains. However, LDL particle diameters (as judged by peaks of LDL-cholesterol profiles) did segregate with progenitors in 29/33 (88%) of RI strains suggesting that a major gene may affect LDL size. In attempting to identify a major LDL-size determining gene, we compared apoB gene restriction fragment length polymorphisms (RFLPs) to the distributions of peak LDL sizes in RI strains. Concordance rates of peak LDL sizes to apoB gene polymorphisms were 18/22 (82%) for the EcoRV RFLP, 5/7 (71%) for HindIII RFLP, and 23/29 (79%) for both (range of P values 0.90-0.95). Thus we could not unequivocally implicate the apoB gene in determining the size of LDL particles. In summary, the genetic control of LDL sizes is more complicated than is the case for HDL; however, the differences in LDL size among these strains of mice may be controlled by a major, as yet unidentified, gene."	J Lipid Res	1990	Mar	"Jiao S, Cole TG, Kitchens RT, Pfleger B, Schonfeld G."	1971301	8 - 10 weeks	female		B = C57BL/6J; H =C3H/HeJ			B	B	H	H	H	B	H	intermediate LDL size of progenitors			H	H
"Inheritance of EcoRV apoB gene polymorphism, LDL size polymorphism, and other chromosome 12 markers"	Rnr - 12	Genetic heterogeneity of plasma lipoproteins in the mouse: control of low density lipoprotein particle sizes by genetic factors.	"In order to assess the genetic control of sizes and concentrations of mouse plasma low density (LDL) and high density lipoproteins (HDL), we used gel permeation fast protein liquid chromatography (FPLC) and nondenaturing gradient polyacrylamide gel electrophoresis to measure the particle sizes of LDL and HDL. Using chromatography we also quantified LDL-cholesterol and HDL-cholesterol concentrations in plasma and used them as indexes of plasma concentrations of the respective particles among 10 inbred strains (AKR/J, BALB/cByJ, C3H/HeJ, C57BL/6J, C57BL/6ByJ, C57L/J, DBA/1LacJ, 129/J, NZB/BINJ, SWR/J) and three sets of recombinant inbred (RI) strains (AKXL/TyJ, BXH/TyJ, CXB/ByJ) of mice. HDL had a dichotomous distribution among the 10 inbred strains. One group had large HDL particle sizes and high HDL-cholesterol concentrations. Another group had smaller HDL particles and lower HDL-cholesterol concentrations, and HDL sizes and HDL-cholesterol concentrations were significantly correlated. In the RI strains, HDL sizes and HDL-cholesterol cholesterol concentrations clearly segregated with one or another of the progenitor strains, and RI strain distributions showed a strong linkage to the apolipoprotein (apo) A-II gene (Apoa-2). In contrast, LDL-cholesterol concentrations and particle sizes on FPLC did not show dichotomous distributions among the 10 inbred strains. In RI strains, the configuration of the LDL FPLC profiles and LDL-cholesterol concentrations did resemble one or another of the progenitors in the majority of cases, but LDLs of several RI strains resembled neither progenitor strain in profile configuration, and LDL-cholesterol concentrations were both greater and smaller than those of progenitor strains. However, LDL particle diameters (as judged by peaks of LDL-cholesterol profiles) did segregate with progenitors in 29/33 (88%) of RI strains suggesting that a major gene may affect LDL size. In attempting to identify a major LDL-size determining gene, we compared apoB gene restriction fragment length polymorphisms (RFLPs) to the distributions of peak LDL sizes in RI strains. Concordance rates of peak LDL sizes to apoB gene polymorphisms were 18/22 (82%) for the EcoRV RFLP, 5/7 (71%) for HindIII RFLP, and 23/29 (79%) for both (range of P values 0.90-0.95). Thus we could not unequivocally implicate the apoB gene in determining the size of LDL particles. In summary, the genetic control of LDL sizes is more complicated than is the case for HDL; however, the differences in LDL size among these strains of mice may be controlled by a major, as yet unidentified, gene."	J Lipid Res	1990	Mar	"Jiao S, Cole TG, Kitchens RT, Pfleger B, Schonfeld G."	1971301	8 - 10 weeks	female		B = C57BL/6J; H =C3H/HeJ			B	B	B	H	H	B	H	H			H	H
"Inheritance of EcoRV apoB gene polymorphism, LDL size polymorphism, and other chromosome 12 markers"	Apob	Genetic heterogeneity of plasma lipoproteins in the mouse: control of low density lipoprotein particle sizes by genetic factors.	"In order to assess the genetic control of sizes and concentrations of mouse plasma low density (LDL) and high density lipoproteins (HDL), we used gel permeation fast protein liquid chromatography (FPLC) and nondenaturing gradient polyacrylamide gel electrophoresis to measure the particle sizes of LDL and HDL. Using chromatography we also quantified LDL-cholesterol and HDL-cholesterol concentrations in plasma and used them as indexes of plasma concentrations of the respective particles among 10 inbred strains (AKR/J, BALB/cByJ, C3H/HeJ, C57BL/6J, C57BL/6ByJ, C57L/J, DBA/1LacJ, 129/J, NZB/BINJ, SWR/J) and three sets of recombinant inbred (RI) strains (AKXL/TyJ, BXH/TyJ, CXB/ByJ) of mice. HDL had a dichotomous distribution among the 10 inbred strains. One group had large HDL particle sizes and high HDL-cholesterol concentrations. Another group had smaller HDL particles and lower HDL-cholesterol concentrations, and HDL sizes and HDL-cholesterol concentrations were significantly correlated. In the RI strains, HDL sizes and HDL-cholesterol cholesterol concentrations clearly segregated with one or another of the progenitor strains, and RI strain distributions showed a strong linkage to the apolipoprotein (apo) A-II gene (Apoa-2). In contrast, LDL-cholesterol concentrations and particle sizes on FPLC did not show dichotomous distributions among the 10 inbred strains. In RI strains, the configuration of the LDL FPLC profiles and LDL-cholesterol concentrations did resemble one or another of the progenitors in the majority of cases, but LDLs of several RI strains resembled neither progenitor strain in profile configuration, and LDL-cholesterol concentrations were both greater and smaller than those of progenitor strains. However, LDL particle diameters (as judged by peaks of LDL-cholesterol profiles) did segregate with progenitors in 29/33 (88%) of RI strains suggesting that a major gene may affect LDL size. In attempting to identify a major LDL-size determining gene, we compared apoB gene restriction fragment length polymorphisms (RFLPs) to the distributions of peak LDL sizes in RI strains. Concordance rates of peak LDL sizes to apoB gene polymorphisms were 18/22 (82%) for the EcoRV RFLP, 5/7 (71%) for HindIII RFLP, and 23/29 (79%) for both (range of P values 0.90-0.95). Thus we could not unequivocally implicate the apoB gene in determining the size of LDL particles. In summary, the genetic control of LDL sizes is more complicated than is the case for HDL; however, the differences in LDL size among these strains of mice may be controlled by a major, as yet unidentified, gene."	J Lipid Res	1990	Mar	"Jiao S, Cole TG, Kitchens RT, Pfleger B, Schonfeld G."	1971301	8 - 10 weeks	female		B = C57BL/6J; H =C3H/HeJ			B	B	B	H	H	B	H	H			H	H
"Inheritance of EcoRV apoB gene polymorphism, LDL size polymorphism, and other chromosome 12 markers"	D12Nyu2	Genetic heterogeneity of plasma lipoproteins in the mouse: control of low density lipoprotein particle sizes by genetic factors.	"In order to assess the genetic control of sizes and concentrations of mouse plasma low density (LDL) and high density lipoproteins (HDL), we used gel permeation fast protein liquid chromatography (FPLC) and nondenaturing gradient polyacrylamide gel electrophoresis to measure the particle sizes of LDL and HDL. Using chromatography we also quantified LDL-cholesterol and HDL-cholesterol concentrations in plasma and used them as indexes of plasma concentrations of the respective particles among 10 inbred strains (AKR/J, BALB/cByJ, C3H/HeJ, C57BL/6J, C57BL/6ByJ, C57L/J, DBA/1LacJ, 129/J, NZB/BINJ, SWR/J) and three sets of recombinant inbred (RI) strains (AKXL/TyJ, BXH/TyJ, CXB/ByJ) of mice. HDL had a dichotomous distribution among the 10 inbred strains. One group had large HDL particle sizes and high HDL-cholesterol concentrations. Another group had smaller HDL particles and lower HDL-cholesterol concentrations, and HDL sizes and HDL-cholesterol concentrations were significantly correlated. In the RI strains, HDL sizes and HDL-cholesterol cholesterol concentrations clearly segregated with one or another of the progenitor strains, and RI strain distributions showed a strong linkage to the apolipoprotein (apo) A-II gene (Apoa-2). In contrast, LDL-cholesterol concentrations and particle sizes on FPLC did not show dichotomous distributions among the 10 inbred strains. In RI strains, the configuration of the LDL FPLC profiles and LDL-cholesterol concentrations did resemble one or another of the progenitors in the majority of cases, but LDLs of several RI strains resembled neither progenitor strain in profile configuration, and LDL-cholesterol concentrations were both greater and smaller than those of progenitor strains. However, LDL particle diameters (as judged by peaks of LDL-cholesterol profiles) did segregate with progenitors in 29/33 (88%) of RI strains suggesting that a major gene may affect LDL size. In attempting to identify a major LDL-size determining gene, we compared apoB gene restriction fragment length polymorphisms (RFLPs) to the distributions of peak LDL sizes in RI strains. Concordance rates of peak LDL sizes to apoB gene polymorphisms were 18/22 (82%) for the EcoRV RFLP, 5/7 (71%) for HindIII RFLP, and 23/29 (79%) for both (range of P values 0.90-0.95). Thus we could not unequivocally implicate the apoB gene in determining the size of LDL particles. In summary, the genetic control of LDL sizes is more complicated than is the case for HDL; however, the differences in LDL size among these strains of mice may be controlled by a major, as yet unidentified, gene."	J Lipid Res	1990	Mar	"Jiao S, Cole TG, Kitchens RT, Pfleger B, Schonfeld G."	1971301	8 - 10 weeks	female		B = C57BL/6J; H =C3H/HeJ			B	B	B	H	H	B	H	B			H	H
"Inheritance of EcoRV apoB gene polymorphism, LDL size polymorphism, and other chromosome 12 markers"	Ly - 18	Genetic heterogeneity of plasma lipoproteins in the mouse: control of low density lipoprotein particle sizes by genetic factors.	"In order to assess the genetic control of sizes and concentrations of mouse plasma low density (LDL) and high density lipoproteins (HDL), we used gel permeation fast protein liquid chromatography (FPLC) and nondenaturing gradient polyacrylamide gel electrophoresis to measure the particle sizes of LDL and HDL. Using chromatography we also quantified LDL-cholesterol and HDL-cholesterol concentrations in plasma and used them as indexes of plasma concentrations of the respective particles among 10 inbred strains (AKR/J, BALB/cByJ, C3H/HeJ, C57BL/6J, C57BL/6ByJ, C57L/J, DBA/1LacJ, 129/J, NZB/BINJ, SWR/J) and three sets of recombinant inbred (RI) strains (AKXL/TyJ, BXH/TyJ, CXB/ByJ) of mice. HDL had a dichotomous distribution among the 10 inbred strains. One group had large HDL particle sizes and high HDL-cholesterol concentrations. Another group had smaller HDL particles and lower HDL-cholesterol concentrations, and HDL sizes and HDL-cholesterol concentrations were significantly correlated. In the RI strains, HDL sizes and HDL-cholesterol cholesterol concentrations clearly segregated with one or another of the progenitor strains, and RI strain distributions showed a strong linkage to the apolipoprotein (apo) A-II gene (Apoa-2). In contrast, LDL-cholesterol concentrations and particle sizes on FPLC did not show dichotomous distributions among the 10 inbred strains. In RI strains, the configuration of the LDL FPLC profiles and LDL-cholesterol concentrations did resemble one or another of the progenitors in the majority of cases, but LDLs of several RI strains resembled neither progenitor strain in profile configuration, and LDL-cholesterol concentrations were both greater and smaller than those of progenitor strains. However, LDL particle diameters (as judged by peaks of LDL-cholesterol profiles) did segregate with progenitors in 29/33 (88%) of RI strains suggesting that a major gene may affect LDL size. In attempting to identify a major LDL-size determining gene, we compared apoB gene restriction fragment length polymorphisms (RFLPs) to the distributions of peak LDL sizes in RI strains. Concordance rates of peak LDL sizes to apoB gene polymorphisms were 18/22 (82%) for the EcoRV RFLP, 5/7 (71%) for HindIII RFLP, and 23/29 (79%) for both (range of P values 0.90-0.95). Thus we could not unequivocally implicate the apoB gene in determining the size of LDL particles. In summary, the genetic control of LDL sizes is more complicated than is the case for HDL; however, the differences in LDL size among these strains of mice may be controlled by a major, as yet unidentified, gene."	J Lipid Res	1990	Mar	"Jiao S, Cole TG, Kitchens RT, Pfleger B, Schonfeld G."	1971301	8 - 10 weeks	female		B = C57BL/6J; H =C3H/HeJ			B	B	B	B	H	B	H	B			H	H
parity distribution of virus - specific RNA in BXH mouse strains	Virus specific RNA:  primiparous	Cellular genes in the mouse regulate in trans the expression of endogenous mouse mammary tumor viruses.	"The transcriptional activities of the eleven mouse mammary tumor virus (MMTV) proviruses endogenous to two sets of recombinant inbred (RI) mouse strains, BXD and BXH, were characterized. Comparison of the levels of virus-specific RNA quantitated in each strain showed no direct relationship between the presence of a particular endogenous provirus or with increasing numbers of proviruses. Association of specific genetic markers with the level of MMTV-specific RNA was examined by using multiple regression analysis. Several cellular loci as well as proviral loci were identified that were significantly associated with viral expression. Importantly, these cellular loci associated with MMTV expression segregated independently of viral sequences."	Genetics	1985	Nov	"Traina-Dorge VL, Carr JK, Bailey-Wilson JE, Elston RC, Taylor BA, Cohen JC."	2996982	3 - 9 months	female		%	0.0265	0.0017	0.0073	0.0152	0.0267	0.0077	0	0.0013	0.024	0.0061	0.012	0.0048	0.096	0.032
parity distribution of virus - specific RNA in BXH mouse strains	Virus specific RNA:  multiparous	Cellular genes in the mouse regulate in trans the expression of endogenous mouse mammary tumor viruses.	"The transcriptional activities of the eleven mouse mammary tumor virus (MMTV) proviruses endogenous to two sets of recombinant inbred (RI) mouse strains, BXD and BXH, were characterized. Comparison of the levels of virus-specific RNA quantitated in each strain showed no direct relationship between the presence of a particular endogenous provirus or with increasing numbers of proviruses. Association of specific genetic markers with the level of MMTV-specific RNA was examined by using multiple regression analysis. Several cellular loci as well as proviral loci were identified that were significantly associated with viral expression. Importantly, these cellular loci associated with MMTV expression segregated independently of viral sequences."	Genetics	1985	Nov	"Traina-Dorge VL, Carr JK, Bailey-Wilson JE, Elston RC, Taylor BA, Cohen JC."	2996982	3 - 9 months	female		%	0.024			0.032	0.036	0.0064	0	0.024	0.032	0.24	0.0086	0.0067	0.06	0.0746
Distribution of MMTV proviruses in BXH mouse strains	Mtv- loci:  1	Cellular genes in the mouse regulate in trans the expression of endogenous mouse mammary tumor viruses.	"The transcriptional activities of the eleven mouse mammary tumor virus (MMTV) proviruses endogenous to two sets of recombinant inbred (RI) mouse strains, BXD and BXH, were characterized. Comparison of the levels of virus-specific RNA quantitated in each strain showed no direct relationship between the presence of a particular endogenous provirus or with increasing numbers of proviruses. Association of specific genetic markers with the level of MMTV-specific RNA was examined by using multiple regression analysis. Several cellular loci as well as proviral loci were identified that were significantly associated with viral expression. Importantly, these cellular loci associated with MMTV expression segregated independently of viral sequences."	Genetics	1985	Nov	"Traina-Dorge VL, Carr JK, Bailey-Wilson JE, Elston RC, Taylor BA, Cohen JC."	2996982	3 - 9 months	female			-	+	+	+	+	+	-	+	-	+	+	+	+	+
Distribution of MMTV proviruses in BXH mouse strains	Mtv- loci:  6	Cellular genes in the mouse regulate in trans the expression of endogenous mouse mammary tumor viruses.	"The transcriptional activities of the eleven mouse mammary tumor virus (MMTV) proviruses endogenous to two sets of recombinant inbred (RI) mouse strains, BXD and BXH, were characterized. Comparison of the levels of virus-specific RNA quantitated in each strain showed no direct relationship between the presence of a particular endogenous provirus or with increasing numbers of proviruses. Association of specific genetic markers with the level of MMTV-specific RNA was examined by using multiple regression analysis. Several cellular loci as well as proviral loci were identified that were significantly associated with viral expression. Importantly, these cellular loci associated with MMTV expression segregated independently of viral sequences."	Genetics	1985	Nov	"Traina-Dorge VL, Carr JK, Bailey-Wilson JE, Elston RC, Taylor BA, Cohen JC."	2996982	3 - 9 months	female			-	+	+	-	+	+	-	+	-	-	+	+	+	+
Distribution of MMTV proviruses in BXH mouse strains	Mtv- loci:  8	Cellular genes in the mouse regulate in trans the expression of endogenous mouse mammary tumor viruses.	"The transcriptional activities of the eleven mouse mammary tumor virus (MMTV) proviruses endogenous to two sets of recombinant inbred (RI) mouse strains, BXD and BXH, were characterized. Comparison of the levels of virus-specific RNA quantitated in each strain showed no direct relationship between the presence of a particular endogenous provirus or with increasing numbers of proviruses. Association of specific genetic markers with the level of MMTV-specific RNA was examined by using multiple regression analysis. Several cellular loci as well as proviral loci were identified that were significantly associated with viral expression. Importantly, these cellular loci associated with MMTV expression segregated independently of viral sequences."	Genetics	1985	Nov	"Traina-Dorge VL, Carr JK, Bailey-Wilson JE, Elston RC, Taylor BA, Cohen JC."	2996982	3 - 9 months	female			+	+	+	+	+	+	+	+	+	+	+	+	+	+
Distribution of MMTV proviruses in BXH mouse strains	Mtv- loci:  9	Cellular genes in the mouse regulate in trans the expression of endogenous mouse mammary tumor viruses.	"The transcriptional activities of the eleven mouse mammary tumor virus (MMTV) proviruses endogenous to two sets of recombinant inbred (RI) mouse strains, BXD and BXH, were characterized. Comparison of the levels of virus-specific RNA quantitated in each strain showed no direct relationship between the presence of a particular endogenous provirus or with increasing numbers of proviruses. Association of specific genetic markers with the level of MMTV-specific RNA was examined by using multiple regression analysis. Several cellular loci as well as proviral loci were identified that were significantly associated with viral expression. Importantly, these cellular loci associated with MMTV expression segregated independently of viral sequences."	Genetics	1985	Nov	"Traina-Dorge VL, Carr JK, Bailey-Wilson JE, Elston RC, Taylor BA, Cohen JC."	2996982	3 - 9 months	female			+	-	+	+	+	+	-	+	+	-	+	-	-	+
Distribution of MMTV proviruses in BXH mouse strains	Mtv- loci:  11	Cellular genes in the mouse regulate in trans the expression of endogenous mouse mammary tumor viruses.	"The transcriptional activities of the eleven mouse mammary tumor virus (MMTV) proviruses endogenous to two sets of recombinant inbred (RI) mouse strains, BXD and BXH, were characterized. Comparison of the levels of virus-specific RNA quantitated in each strain showed no direct relationship between the presence of a particular endogenous provirus or with increasing numbers of proviruses. Association of specific genetic markers with the level of MMTV-specific RNA was examined by using multiple regression analysis. Several cellular loci as well as proviral loci were identified that were significantly associated with viral expression. Importantly, these cellular loci associated with MMTV expression segregated independently of viral sequences."	Genetics	1985	Nov	"Traina-Dorge VL, Carr JK, Bailey-Wilson JE, Elston RC, Taylor BA, Cohen JC."	2996982	3 - 9 months	female			-	+	+	-	+	-	-	-	-	-	+	+	+	+
Distribution of MMTV proviruses in BXH mouse strains	Mtv- loci:  14	Cellular genes in the mouse regulate in trans the expression of endogenous mouse mammary tumor viruses.	"The transcriptional activities of the eleven mouse mammary tumor virus (MMTV) proviruses endogenous to two sets of recombinant inbred (RI) mouse strains, BXD and BXH, were characterized. Comparison of the levels of virus-specific RNA quantitated in each strain showed no direct relationship between the presence of a particular endogenous provirus or with increasing numbers of proviruses. Association of specific genetic markers with the level of MMTV-specific RNA was examined by using multiple regression analysis. Several cellular loci as well as proviral loci were identified that were significantly associated with viral expression. Importantly, these cellular loci associated with MMTV expression segregated independently of viral sequences."	Genetics	1985	Nov	"Traina-Dorge VL, Carr JK, Bailey-Wilson JE, Elston RC, Taylor BA, Cohen JC."	2996982	3 - 9 months	female			-	+	-	-	-	+	+	+	-	-	+	-	-	-
Distribution of MMTV proviruses in BXH mouse strains	Total Proviruses	Cellular genes in the mouse regulate in trans the expression of endogenous mouse mammary tumor viruses.	"The transcriptional activities of the eleven mouse mammary tumor virus (MMTV) proviruses endogenous to two sets of recombinant inbred (RI) mouse strains, BXD and BXH, were characterized. Comparison of the levels of virus-specific RNA quantitated in each strain showed no direct relationship between the presence of a particular endogenous provirus or with increasing numbers of proviruses. Association of specific genetic markers with the level of MMTV-specific RNA was examined by using multiple regression analysis. Several cellular loci as well as proviral loci were identified that were significantly associated with viral expression. Importantly, these cellular loci associated with MMTV expression segregated independently of viral sequences."	Genetics	1985	Nov	"Traina-Dorge VL, Carr JK, Bailey-Wilson JE, Elston RC, Taylor BA, Cohen JC."	2996982	3 - 9 months	female			2	5	5	3	5	5	2	5	2	2	6	4	4	5
SDP of alleles of Sap and Linked Loci in RI strains	Ly - 17	Chromosomal location of the gene encoding the murine acute-phase protein serum amyloid P-component (SAP).	"A full-length cDNA clone, pmSAP3, encoding, the serum P component (SAP), has been used to search for DNA fragment length variation among mouse strains previously analyzed for differences in endogenous SAP levels. Three alleles were found using EcoRI-digested DNA. The finding of a single 5.4-kb fragment, allele d, in DNA from DBA/2J mice suggests the presence of a single Sap locus. Segregation of DNA fragment associated with Sapb and Sapd alleles was analyzed in three sets of recombinant inbred (RI) strains. The strain distribution pattern found for the Sap alleles was identical to that of alleles of Ly-9 in 43 individual RI strains, suggesting tight linkage with Ly-9 on mouse chromosome 1. In the BXD RI strains, the SDP of the Sap locus, defined by the difference in the endogenous SAP level, is also identical to the SDP of the DNA fragments. We propose to redesignate the Sap locus to include both the structural element defined by the DNA polymorphism and the regulatory element involved in the regulation of SAP synthesis. The Sap locus is the major genetic element contributing to the regulation of SAP production. Other genetic factors are also involved, as shown by the presence of nonparental phenotypes in the individual BXH RI strains."	Biochem Genet	1989	Apr	"Maruyama N, Shigemoto K, Kubo S, Handa S, Ishikawa N, Itoh Y, Elliott RW"	2570566		both		B = C57BL/6J; H =C3H/HeJ			B	B	B	H	B	B	H	B	B	H	H	B
SDP of alleles of Sap and Linked Loci in RI strains	Ly - 9/Sap	Chromosomal location of the gene encoding the murine acute-phase protein serum amyloid P-component (SAP).	"A full-length cDNA clone, pmSAP3, encoding, the serum P component (SAP), has been used to search for DNA fragment length variation among mouse strains previously analyzed for differences in endogenous SAP levels. Three alleles were found using EcoRI-digested DNA. The finding of a single 5.4-kb fragment, allele d, in DNA from DBA/2J mice suggests the presence of a single Sap locus. Segregation of DNA fragment associated with Sapb and Sapd alleles was analyzed in three sets of recombinant inbred (RI) strains. The strain distribution pattern found for the Sap alleles was identical to that of alleles of Ly-9 in 43 individual RI strains, suggesting tight linkage with Ly-9 on mouse chromosome 1. In the BXD RI strains, the SDP of the Sap locus, defined by the difference in the endogenous SAP level, is also identical to the SDP of the DNA fragments. We propose to redesignate the Sap locus to include both the structural element defined by the DNA polymorphism and the regulatory element involved in the regulation of SAP synthesis. The Sap locus is the major genetic element contributing to the regulation of SAP production. Other genetic factors are also involved, as shown by the presence of nonparental phenotypes in the individual BXH RI strains."	Biochem Genet	1989	Apr	"Maruyama N, Shigemoto K, Kubo S, Handa S, Ishikawa N, Itoh Y, Elliott RW"	2570566		both		B = C57BL/6J; H =C3H/HeJ			B	H	B	H	B	B	H	B	H	H	H	B
SDP of alleles of Sap and Linked Loci in RI strains	Spna - 1	Chromosomal location of the gene encoding the murine acute-phase protein serum amyloid P-component (SAP).	"A full-length cDNA clone, pmSAP3, encoding, the serum P component (SAP), has been used to search for DNA fragment length variation among mouse strains previously analyzed for differences in endogenous SAP levels. Three alleles were found using EcoRI-digested DNA. The finding of a single 5.4-kb fragment, allele d, in DNA from DBA/2J mice suggests the presence of a single Sap locus. Segregation of DNA fragment associated with Sapb and Sapd alleles was analyzed in three sets of recombinant inbred (RI) strains. The strain distribution pattern found for the Sap alleles was identical to that of alleles of Ly-9 in 43 individual RI strains, suggesting tight linkage with Ly-9 on mouse chromosome 1. In the BXD RI strains, the SDP of the Sap locus, defined by the difference in the endogenous SAP level, is also identical to the SDP of the DNA fragments. We propose to redesignate the Sap locus to include both the structural element defined by the DNA polymorphism and the regulatory element involved in the regulation of SAP synthesis. The Sap locus is the major genetic element contributing to the regulation of SAP production. Other genetic factors are also involved, as shown by the presence of nonparental phenotypes in the individual BXH RI strains."	Biochem Genet	1989	Apr	"Maruyama N, Shigemoto K, Kubo S, Handa S, Ishikawa N, Itoh Y, Elliott RW"	2570566		both		B = C57BL/6J; H =C3H/HeJ			B	B	B	H	B	B	H	B	H	H	H	B
Phenotyping of BXH strains	LPS Phenotype	The physical separation of Lps and Ifa loci in BXH recombinant inbred mice.	"Several reports in the literature suggest that many of the phenotypic defects of LPS-hyporesponsive C3H/HeJ mice may be attributed to decreased IFN production by their macrophages. The physical proximity on chromosome 4 of the gene which encodes sensitivity to LPS (Lps) and the structural gene cluster which encodes IFN-alpha (Ifa), suggests the possibility that the Lps gene, whose product is unknown, may actually be a part of the Ifa gene cluster. The C57BL/6J and C3H/HeJ mouse strains carry distinct alleles at both the LPs and the Ifa loci. In this study, we have analyzed these parental strains, as well as 12 recombinant inbred strains derived from these parental strains (e.g., BXH strains), for inheritance of these distinct alleles. The results show the segregation of these two loci: in 5 of 12 BXH RI strains, the IFN-alpha restriction fragment length polymorphism characteristic of one parental strain was discordant with the predicted LPS response phenotype. Therefore, we conclude that the Lps and the Ifa genes are physically distinct despite the apparent cause and effect relationship which is observed phenotypically."	J Immunol	1989	Nov	"Fultz MJ, Vogel SN."	2572648		both		B = C57BL/6J; H =C3H/HeJ	B	H	H	H	H	H	H	H	H	B	B	H	B	
Phenotyping of BXH strains	VSV Phenotype	The physical separation of Lps and Ifa loci in BXH recombinant inbred mice.	"Several reports in the literature suggest that many of the phenotypic defects of LPS-hyporesponsive C3H/HeJ mice may be attributed to decreased IFN production by their macrophages. The physical proximity on chromosome 4 of the gene which encodes sensitivity to LPS (Lps) and the structural gene cluster which encodes IFN-alpha (Ifa), suggests the possibility that the Lps gene, whose product is unknown, may actually be a part of the Ifa gene cluster. The C57BL/6J and C3H/HeJ mouse strains carry distinct alleles at both the LPs and the Ifa loci. In this study, we have analyzed these parental strains, as well as 12 recombinant inbred strains derived from these parental strains (e.g., BXH strains), for inheritance of these distinct alleles. The results show the segregation of these two loci: in 5 of 12 BXH RI strains, the IFN-alpha restriction fragment length polymorphism characteristic of one parental strain was discordant with the predicted LPS response phenotype. Therefore, we conclude that the Lps and the Ifa genes are physically distinct despite the apparent cause and effect relationship which is observed phenotypically."	J Immunol	1989	Nov	"Fultz MJ, Vogel SN."	2572648		both		B = C57BL/6J; H =C3H/HeJ	B	H	H	H	H	H	H	H	H			H	B	
Phenotyping of BXH strains	IFN- alpha Phenotype	The physical separation of Lps and Ifa loci in BXH recombinant inbred mice.	"Several reports in the literature suggest that many of the phenotypic defects of LPS-hyporesponsive C3H/HeJ mice may be attributed to decreased IFN production by their macrophages. The physical proximity on chromosome 4 of the gene which encodes sensitivity to LPS (Lps) and the structural gene cluster which encodes IFN-alpha (Ifa), suggests the possibility that the Lps gene, whose product is unknown, may actually be a part of the Ifa gene cluster. The C57BL/6J and C3H/HeJ mouse strains carry distinct alleles at both the LPs and the Ifa loci. In this study, we have analyzed these parental strains, as well as 12 recombinant inbred strains derived from these parental strains (e.g., BXH strains), for inheritance of these distinct alleles. The results show the segregation of these two loci: in 5 of 12 BXH RI strains, the IFN-alpha restriction fragment length polymorphism characteristic of one parental strain was discordant with the predicted LPS response phenotype. Therefore, we conclude that the Lps and the Ifa genes are physically distinct despite the apparent cause and effect relationship which is observed phenotypically."	J Immunol	1989	Nov	"Fultz MJ, Vogel SN."	2572648		both		B = C57BL/6J; H =C3H/HeJ	B	H	H	B	H	B	B	B	H	B	B	H	B	
IFN - alpha strain distribution patterns	Parental or BXH Strain Designation - Endonuclease:  StuI	The physical separation of Lps and Ifa loci in BXH recombinant inbred mice.	"Several reports in the literature suggest that many of the phenotypic defects of LPS-hyporesponsive C3H/HeJ mice may be attributed to decreased IFN production by their macrophages. The physical proximity on chromosome 4 of the gene which encodes sensitivity to LPS (Lps) and the structural gene cluster which encodes IFN-alpha (Ifa), suggests the possibility that the Lps gene, whose product is unknown, may actually be a part of the Ifa gene cluster. The C57BL/6J and C3H/HeJ mouse strains carry distinct alleles at both the LPs and the Ifa loci. In this study, we have analyzed these parental strains, as well as 12 recombinant inbred strains derived from these parental strains (e.g., BXH strains), for inheritance of these distinct alleles. The results show the segregation of these two loci: in 5 of 12 BXH RI strains, the IFN-alpha restriction fragment length polymorphism characteristic of one parental strain was discordant with the predicted LPS response phenotype. Therefore, we conclude that the Lps and the Ifa genes are physically distinct despite the apparent cause and effect relationship which is observed phenotypically."	J Immunol	1989	Nov	"Fultz MJ, Vogel SN."	2572648		both		B = C57BL/6J; H =C3H/HeJ	B	H	H	B	H		B	B	H	B	B	H	B	H
IFN - alpha strain distribution patterns	Parental or BXH Strain Designation - Endonuclease: PvuII/SphI	The physical separation of Lps and Ifa loci in BXH recombinant inbred mice.	"Several reports in the literature suggest that many of the phenotypic defects of LPS-hyporesponsive C3H/HeJ mice may be attributed to decreased IFN production by their macrophages. The physical proximity on chromosome 4 of the gene which encodes sensitivity to LPS (Lps) and the structural gene cluster which encodes IFN-alpha (Ifa), suggests the possibility that the Lps gene, whose product is unknown, may actually be a part of the Ifa gene cluster. The C57BL/6J and C3H/HeJ mouse strains carry distinct alleles at both the LPs and the Ifa loci. In this study, we have analyzed these parental strains, as well as 12 recombinant inbred strains derived from these parental strains (e.g., BXH strains), for inheritance of these distinct alleles. The results show the segregation of these two loci: in 5 of 12 BXH RI strains, the IFN-alpha restriction fragment length polymorphism characteristic of one parental strain was discordant with the predicted LPS response phenotype. Therefore, we conclude that the Lps and the Ifa genes are physically distinct despite the apparent cause and effect relationship which is observed phenotypically."	J Immunol	1989	Nov	"Fultz MJ, Vogel SN."	2572648		both		B = C57BL/6J; H =C3H/HeJ	B	H	H	B	H	B	B	B	H	B	B	H	B	H
IFN - alpha strain distribution patterns	Parental or BXH Strain Designation - Endonuclease:  EcoRI	The physical separation of Lps and Ifa loci in BXH recombinant inbred mice.	"Several reports in the literature suggest that many of the phenotypic defects of LPS-hyporesponsive C3H/HeJ mice may be attributed to decreased IFN production by their macrophages. The physical proximity on chromosome 4 of the gene which encodes sensitivity to LPS (Lps) and the structural gene cluster which encodes IFN-alpha (Ifa), suggests the possibility that the Lps gene, whose product is unknown, may actually be a part of the Ifa gene cluster. The C57BL/6J and C3H/HeJ mouse strains carry distinct alleles at both the LPs and the Ifa loci. In this study, we have analyzed these parental strains, as well as 12 recombinant inbred strains derived from these parental strains (e.g., BXH strains), for inheritance of these distinct alleles. The results show the segregation of these two loci: in 5 of 12 BXH RI strains, the IFN-alpha restriction fragment length polymorphism characteristic of one parental strain was discordant with the predicted LPS response phenotype. Therefore, we conclude that the Lps and the Ifa genes are physically distinct despite the apparent cause and effect relationship which is observed phenotypically."	J Immunol	1989	Nov	"Fultz MJ, Vogel SN."	2572648		both		B = C57BL/6J; H =C3H/HeJ	B	H	H	B	H	B	B	B	H	B	B			H
IFN - alpha strain distribution patterns	Parental or BXH Strain Designation - Endonuclease:  HindIII/PstI/BgII	The physical separation of Lps and Ifa loci in BXH recombinant inbred mice.	"Several reports in the literature suggest that many of the phenotypic defects of LPS-hyporesponsive C3H/HeJ mice may be attributed to decreased IFN production by their macrophages. The physical proximity on chromosome 4 of the gene which encodes sensitivity to LPS (Lps) and the structural gene cluster which encodes IFN-alpha (Ifa), suggests the possibility that the Lps gene, whose product is unknown, may actually be a part of the Ifa gene cluster. The C57BL/6J and C3H/HeJ mouse strains carry distinct alleles at both the LPs and the Ifa loci. In this study, we have analyzed these parental strains, as well as 12 recombinant inbred strains derived from these parental strains (e.g., BXH strains), for inheritance of these distinct alleles. The results show the segregation of these two loci: in 5 of 12 BXH RI strains, the IFN-alpha restriction fragment length polymorphism characteristic of one parental strain was discordant with the predicted LPS response phenotype. Therefore, we conclude that the Lps and the Ifa genes are physically distinct despite the apparent cause and effect relationship which is observed phenotypically."	J Immunol	1989	Nov	"Fultz MJ, Vogel SN."	2572648		both		B = C57BL/6J; H =C3H/HeJ	B	H	H	B	H	B			H		B	H	B	H
IFN - alpha strain distribution patterns	Parental or BXH Strain Designation - Endonuclease:  EcoRI/BgI II/ BamHI	The physical separation of Lps and Ifa loci in BXH recombinant inbred mice.	"Several reports in the literature suggest that many of the phenotypic defects of LPS-hyporesponsive C3H/HeJ mice may be attributed to decreased IFN production by their macrophages. The physical proximity on chromosome 4 of the gene which encodes sensitivity to LPS (Lps) and the structural gene cluster which encodes IFN-alpha (Ifa), suggests the possibility that the Lps gene, whose product is unknown, may actually be a part of the Ifa gene cluster. The C57BL/6J and C3H/HeJ mouse strains carry distinct alleles at both the LPs and the Ifa loci. In this study, we have analyzed these parental strains, as well as 12 recombinant inbred strains derived from these parental strains (e.g., BXH strains), for inheritance of these distinct alleles. The results show the segregation of these two loci: in 5 of 12 BXH RI strains, the IFN-alpha restriction fragment length polymorphism characteristic of one parental strain was discordant with the predicted LPS response phenotype. Therefore, we conclude that the Lps and the Ifa genes are physically distinct despite the apparent cause and effect relationship which is observed phenotypically."	J Immunol	1989	Nov	"Fultz MJ, Vogel SN."	2572648		both		B = C57BL/6J; H =C3H/HeJ	B	H	H	B	H	B	B	B	H	B	B	H	B	H
Pattern of 6C3 reactivity and frequency of 6C3+ T cells:  association with the Ly - 6 phenotype	6C3 staining pattern	Xenogeneic monoclonal antibody to an Ly-6-linked murine cell surface antigen: differential reactivity with T cell subpopulations and bone marrow cells.	"The patterns of cellular and strain reactivity of a monoclonal antibody (6C3 MAb) derived from the fusion of SP2/0 cells with splenocytes from rats immunized against MRL/MpJ-lpr/lpr T cells were characterized by using flow cytofluorometry (FCF) analysis. This MAb was found to stain 70 to 90% of T cells of mice with the lpr/lpr genotype and 20 to 60% of T cells of congenic +/+ strains. Dual-parameter FCF analysis of Lyt-2 vs 6C3 expression revealed the existence of several Lyt-2- and Lyt-2+ T cell subsets, one of which (Lyt-2- bright 6C3+) was expanded in lpr/lpr-bearing mice. The 6C3 MAb stained only 2 to 5% normal thymocytes but reacted with 40 to 50% bone marrow (BM) cells. A strain survey demonstrated the expression of the 6C3 antigen on peripheral T cells (and BM cells) of all strains examined, with the exception of NOD, NZB/B1NJ, and ST/bJ. Interestingly, in the positive strains, two types of 6C3 staining patterns of T cells were observed: bimodal or trimodal. Study of BXH and CXB recombinant inbred (RI) strains demonstrated that the bimodal and trimodal 6C3 patterns are associated with the Ly-6.1 and Ly-6.2 phenotypes, respectively. Linkage of 6C3 expression with the Ly-6 locus was confirmed by using the congenic C3H.B6-Ly-6b strain. Moreover, the 6C3 staining of T cells in Ly-6.2 strains was reduced by preincubation with the H9/25 and SK-142-446 MAb, which are known to recognize Ly-6.2-associated antigens. Therefore, the 6C3 MAb appears to detect a frame-work determinant on an Ly-6-linked antigen that is absent from T cells of NOD, NZB, and ST/bJ mice. Analysis of (NZB x C58) NX8 RI strains demonstrated a correlation between the lack of 6C3 expression on T cells and unresponsiveness in autologous mixed lymphocyte reaction (a property of NZB/B1NJ mice). The 6C3 MAb should prove useful for further genetic and biochemical analysis of the Ly-6 locus and its product(s), and for the delineation of functional subsets of T cells and BM cells in normal and lpr/lpr-bearing mice."	J Immunol 	1985	Apr	"Dumont FJ, Coker LZ, Habbersett RC, Treffinger JA."	3156181	8 - 16 weeks	both					trimodal	bimodal	trimodal	trimodal	bimodal	bimodal	bimodal	trimodal	trimodal	trimodal	trimodal	bimodal
Pattern of 6C3 reactivity and frequency of 6C3+ T cells:  association with the Ly - 6 phenotype	%6C3 Cells:  dull	Xenogeneic monoclonal antibody to an Ly-6-linked murine cell surface antigen: differential reactivity with T cell subpopulations and bone marrow cells.	"The patterns of cellular and strain reactivity of a monoclonal antibody (6C3 MAb) derived from the fusion of SP2/0 cells with splenocytes from rats immunized against MRL/MpJ-lpr/lpr T cells were characterized by using flow cytofluorometry (FCF) analysis. This MAb was found to stain 70 to 90% of T cells of mice with the lpr/lpr genotype and 20 to 60% of T cells of congenic +/+ strains. Dual-parameter FCF analysis of Lyt-2 vs 6C3 expression revealed the existence of several Lyt-2- and Lyt-2+ T cell subsets, one of which (Lyt-2- bright 6C3+) was expanded in lpr/lpr-bearing mice. The 6C3 MAb stained only 2 to 5% normal thymocytes but reacted with 40 to 50% bone marrow (BM) cells. A strain survey demonstrated the expression of the 6C3 antigen on peripheral T cells (and BM cells) of all strains examined, with the exception of NOD, NZB/B1NJ, and ST/bJ. Interestingly, in the positive strains, two types of 6C3 staining patterns of T cells were observed: bimodal or trimodal. Study of BXH and CXB recombinant inbred (RI) strains demonstrated that the bimodal and trimodal 6C3 patterns are associated with the Ly-6.1 and Ly-6.2 phenotypes, respectively. Linkage of 6C3 expression with the Ly-6 locus was confirmed by using the congenic C3H.B6-Ly-6b strain. Moreover, the 6C3 staining of T cells in Ly-6.2 strains was reduced by preincubation with the H9/25 and SK-142-446 MAb, which are known to recognize Ly-6.2-associated antigens. Therefore, the 6C3 MAb appears to detect a frame-work determinant on an Ly-6-linked antigen that is absent from T cells of NOD, NZB, and ST/bJ mice. Analysis of (NZB x C58) NX8 RI strains demonstrated a correlation between the lack of 6C3 expression on T cells and unresponsiveness in autologous mixed lymphocyte reaction (a property of NZB/B1NJ mice). The 6C3 MAb should prove useful for further genetic and biochemical analysis of the Ly-6 locus and its product(s), and for the delineation of functional subsets of T cells and BM cells in normal and lpr/lpr-bearing mice."	J Immunol 	1985	Apr	"Dumont FJ, Coker LZ, Habbersett RC, Treffinger JA."	3156181	8 - 16 weeks	both		%			28.6		35.7	28.5				36.9	34.2	25.7	32.6	
Pattern of 6C3 reactivity and frequency of 6C3+ T cells:  association with the Ly - 6 phenotype	%6C3 Cells:  bright	Xenogeneic monoclonal antibody to an Ly-6-linked murine cell surface antigen: differential reactivity with T cell subpopulations and bone marrow cells.	"The patterns of cellular and strain reactivity of a monoclonal antibody (6C3 MAb) derived from the fusion of SP2/0 cells with splenocytes from rats immunized against MRL/MpJ-lpr/lpr T cells were characterized by using flow cytofluorometry (FCF) analysis. This MAb was found to stain 70 to 90% of T cells of mice with the lpr/lpr genotype and 20 to 60% of T cells of congenic +/+ strains. Dual-parameter FCF analysis of Lyt-2 vs 6C3 expression revealed the existence of several Lyt-2- and Lyt-2+ T cell subsets, one of which (Lyt-2- bright 6C3+) was expanded in lpr/lpr-bearing mice. The 6C3 MAb stained only 2 to 5% normal thymocytes but reacted with 40 to 50% bone marrow (BM) cells. A strain survey demonstrated the expression of the 6C3 antigen on peripheral T cells (and BM cells) of all strains examined, with the exception of NOD, NZB/B1NJ, and ST/bJ. Interestingly, in the positive strains, two types of 6C3 staining patterns of T cells were observed: bimodal or trimodal. Study of BXH and CXB recombinant inbred (RI) strains demonstrated that the bimodal and trimodal 6C3 patterns are associated with the Ly-6.1 and Ly-6.2 phenotypes, respectively. Linkage of 6C3 expression with the Ly-6 locus was confirmed by using the congenic C3H.B6-Ly-6b strain. Moreover, the 6C3 staining of T cells in Ly-6.2 strains was reduced by preincubation with the H9/25 and SK-142-446 MAb, which are known to recognize Ly-6.2-associated antigens. Therefore, the 6C3 MAb appears to detect a frame-work determinant on an Ly-6-linked antigen that is absent from T cells of NOD, NZB, and ST/bJ mice. Analysis of (NZB x C58) NX8 RI strains demonstrated a correlation between the lack of 6C3 expression on T cells and unresponsiveness in autologous mixed lymphocyte reaction (a property of NZB/B1NJ mice). The 6C3 MAb should prove useful for further genetic and biochemical analysis of the Ly-6 locus and its product(s), and for the delineation of functional subsets of T cells and BM cells in normal and lpr/lpr-bearing mice."	J Immunol 	1985	Apr	"Dumont FJ, Coker LZ, Habbersett RC, Treffinger JA."	3156181	8 - 16 weeks	both		%			10.1	35.2	9.7	8.1	25.2	26.1	30.7	9.7	9.3	9.5	10	21.6
Pattern of 6C3 reactivity and frequency of 6C3+ T cells:  association with the Ly - 6 phenotype	Ly - 6 Allele	Xenogeneic monoclonal antibody to an Ly-6-linked murine cell surface antigen: differential reactivity with T cell subpopulations and bone marrow cells.	"The patterns of cellular and strain reactivity of a monoclonal antibody (6C3 MAb) derived from the fusion of SP2/0 cells with splenocytes from rats immunized against MRL/MpJ-lpr/lpr T cells were characterized by using flow cytofluorometry (FCF) analysis. This MAb was found to stain 70 to 90% of T cells of mice with the lpr/lpr genotype and 20 to 60% of T cells of congenic +/+ strains. Dual-parameter FCF analysis of Lyt-2 vs 6C3 expression revealed the existence of several Lyt-2- and Lyt-2+ T cell subsets, one of which (Lyt-2- bright 6C3+) was expanded in lpr/lpr-bearing mice. The 6C3 MAb stained only 2 to 5% normal thymocytes but reacted with 40 to 50% bone marrow (BM) cells. A strain survey demonstrated the expression of the 6C3 antigen on peripheral T cells (and BM cells) of all strains examined, with the exception of NOD, NZB/B1NJ, and ST/bJ. Interestingly, in the positive strains, two types of 6C3 staining patterns of T cells were observed: bimodal or trimodal. Study of BXH and CXB recombinant inbred (RI) strains demonstrated that the bimodal and trimodal 6C3 patterns are associated with the Ly-6.1 and Ly-6.2 phenotypes, respectively. Linkage of 6C3 expression with the Ly-6 locus was confirmed by using the congenic C3H.B6-Ly-6b strain. Moreover, the 6C3 staining of T cells in Ly-6.2 strains was reduced by preincubation with the H9/25 and SK-142-446 MAb, which are known to recognize Ly-6.2-associated antigens. Therefore, the 6C3 MAb appears to detect a frame-work determinant on an Ly-6-linked antigen that is absent from T cells of NOD, NZB, and ST/bJ mice. Analysis of (NZB x C58) NX8 RI strains demonstrated a correlation between the lack of 6C3 expression on T cells and unresponsiveness in autologous mixed lymphocyte reaction (a property of NZB/B1NJ mice). The 6C3 MAb should prove useful for further genetic and biochemical analysis of the Ly-6 locus and its product(s), and for the delineation of functional subsets of T cells and BM cells in normal and lpr/lpr-bearing mice."	J Immunol 	1985	Apr	"Dumont FJ, Coker LZ, Habbersett RC, Treffinger JA."	3156181	8 - 16 weeks	both					2	1	2	2	1	1	1	2	2	2	2	1
Secondary anti - HEL responses in H-2 Ri mice	PFC/ 10^6 PT - LN	Selective reversal of H-2 linked genetic unresponsiveness to lysozymes. I. Non-H-2 gene(s) closely linked to the Ir-2 locus on chromosome 2 permit(s) an antilysozyme response in H-2b mice.	"Genes outside of the mouse major histocompatibility complex (H-2) were found to be capable of specifically reversing the previously described nonresponsiveness to hen egg-white lysozyme (HEL) owing to H-2b immune response (Ir) genes. C3H.SW, BALB.B, and C57L, all of the H-2b haplotype, showed responsiveness to HEL, but not to human lysozyme (HUL). Mapping of the reversing gene(s) was attempted by testing H-2b recombinant inbred (RI) strains of mice carrying C3H, BALB, and C57L non-H-2 genes. Analysis of the strain distribution pattern of responsiveness with both CXB and BXH RI strains was consistent with the location of the responsible site within the H-3 region on chromosome 2. The anti-HEL proliferative responsiveness in two H-3 congenic strains of mice, B10.C(28NX)SN and B10.C-H-3cH-3a, that have BALB/c genes within the H-3 region confirmed the mapping, as well as localized the reversing gene(s) near the Ir-2 gene. The data are discussed with regard to the site of expression of the reversing gene(s) and its mechanism of action."	Immunogenetics	1984		"Sadegh-Nasseri S, Kipp DE, Taylor BA, Miller A, Sercarz E."	6437975	2 - 6 months	both	26-May	(those with multiple values are bimodal)	1; 170	( C3H.SW)450			38			200	14	310	15			1.1
Secondary anti - HEL responses in H-2 Ri mice	Range	Selective reversal of H-2 linked genetic unresponsiveness to lysozymes. I. Non-H-2 gene(s) closely linked to the Ir-2 locus on chromosome 2 permit(s) an antilysozyme response in H-2b mice.	"Genes outside of the mouse major histocompatibility complex (H-2) were found to be capable of specifically reversing the previously described nonresponsiveness to hen egg-white lysozyme (HEL) owing to H-2b immune response (Ir) genes. C3H.SW, BALB.B, and C57L, all of the H-2b haplotype, showed responsiveness to HEL, but not to human lysozyme (HUL). Mapping of the reversing gene(s) was attempted by testing H-2b recombinant inbred (RI) strains of mice carrying C3H, BALB, and C57L non-H-2 genes. Analysis of the strain distribution pattern of responsiveness with both CXB and BXH RI strains was consistent with the location of the responsible site within the H-3 region on chromosome 2. The anti-HEL proliferative responsiveness in two H-3 congenic strains of mice, B10.C(28NX)SN and B10.C-H-3cH-3a, that have BALB/c genes within the H-3 region confirmed the mapping, as well as localized the reversing gene(s) near the Ir-2 gene. The data are discussed with regard to the site of expression of the reversing gene(s) and its mechanism of action."	Immunogenetics	1984		"Sadegh-Nasseri S, Kipp DE, Taylor BA, Miller A, Sercarz E."	6437975	2 - 6 months	both	26-May	(those with multiple values are bimodal)	<1; 150 - 240	( C3H.SW)167 - 1370			<1 - 110			80 - 520	<1 - 80	21 - 1520	Jun-38			<1 - 3
Secondary anti - HEL responses in H-2 Ri mice	Score	Selective reversal of H-2 linked genetic unresponsiveness to lysozymes. I. Non-H-2 gene(s) closely linked to the Ir-2 locus on chromosome 2 permit(s) an antilysozyme response in H-2b mice.	"Genes outside of the mouse major histocompatibility complex (H-2) were found to be capable of specifically reversing the previously described nonresponsiveness to hen egg-white lysozyme (HEL) owing to H-2b immune response (Ir) genes. C3H.SW, BALB.B, and C57L, all of the H-2b haplotype, showed responsiveness to HEL, but not to human lysozyme (HUL). Mapping of the reversing gene(s) was attempted by testing H-2b recombinant inbred (RI) strains of mice carrying C3H, BALB, and C57L non-H-2 genes. Analysis of the strain distribution pattern of responsiveness with both CXB and BXH RI strains was consistent with the location of the responsible site within the H-3 region on chromosome 2. The anti-HEL proliferative responsiveness in two H-3 congenic strains of mice, B10.C(28NX)SN and B10.C-H-3cH-3a, that have BALB/c genes within the H-3 region confirmed the mapping, as well as localized the reversing gene(s) near the Ir-2 gene. The data are discussed with regard to the site of expression of the reversing gene(s) and its mechanism of action."	Immunogenetics	1984		"Sadegh-Nasseri S, Kipp DE, Taylor BA, Miller A, Sercarz E."	6437975	2 - 6 months	both	26-May	(those with multiple values are bimodal)<5 = 0;  6 - 25 = +/-;  26 - 125 = +;  126 - 625 = ++	0;  ++	 ( C3H.SW)++			+/-			++	+/-	++	+/-			0
Secondary anti - HUL responses in H-2 Ri mice	PFC/ 10^6 PT - LN	Selective reversal of H-2 linked genetic unresponsiveness to lysozymes. I. Non-H-2 gene(s) closely linked to the Ir-2 locus on chromosome 2 permit(s) an antilysozyme response in H-2b mice.	"Genes outside of the mouse major histocompatibility complex (H-2) were found to be capable of specifically reversing the previously described nonresponsiveness to hen egg-white lysozyme (HEL) owing to H-2b immune response (Ir) genes. C3H.SW, BALB.B, and C57L, all of the H-2b haplotype, showed responsiveness to HEL, but not to human lysozyme (HUL). Mapping of the reversing gene(s) was attempted by testing H-2b recombinant inbred (RI) strains of mice carrying C3H, BALB, and C57L non-H-2 genes. Analysis of the strain distribution pattern of responsiveness with both CXB and BXH RI strains was consistent with the location of the responsible site within the H-3 region on chromosome 2. The anti-HEL proliferative responsiveness in two H-3 congenic strains of mice, B10.C(28NX)SN and B10.C-H-3cH-3a, that have BALB/c genes within the H-3 region confirmed the mapping, as well as localized the reversing gene(s) near the Ir-2 gene. The data are discussed with regard to the site of expression of the reversing gene(s) and its mechanism of action."	Immunogenetics	1984		"Sadegh-Nasseri S, Kipp DE, Taylor BA, Miller A, Sercarz E."	6437975	2 - 6 months	both	25-Apr	(those with multiple values are bimodal)	2	 ( C3H.SW)1; 35			4			1; 90	2	15	9			
Secondary anti - HUL responses in H-2 Ri mice	Range	Selective reversal of H-2 linked genetic unresponsiveness to lysozymes. I. Non-H-2 gene(s) closely linked to the Ir-2 locus on chromosome 2 permit(s) an antilysozyme response in H-2b mice.	"Genes outside of the mouse major histocompatibility complex (H-2) were found to be capable of specifically reversing the previously described nonresponsiveness to hen egg-white lysozyme (HEL) owing to H-2b immune response (Ir) genes. C3H.SW, BALB.B, and C57L, all of the H-2b haplotype, showed responsiveness to HEL, but not to human lysozyme (HUL). Mapping of the reversing gene(s) was attempted by testing H-2b recombinant inbred (RI) strains of mice carrying C3H, BALB, and C57L non-H-2 genes. Analysis of the strain distribution pattern of responsiveness with both CXB and BXH RI strains was consistent with the location of the responsible site within the H-3 region on chromosome 2. The anti-HEL proliferative responsiveness in two H-3 congenic strains of mice, B10.C(28NX)SN and B10.C-H-3cH-3a, that have BALB/c genes within the H-3 region confirmed the mapping, as well as localized the reversing gene(s) near the Ir-2 gene. The data are discussed with regard to the site of expression of the reversing gene(s) and its mechanism of action."	Immunogenetics	1984		"Sadegh-Nasseri S, Kipp DE, Taylor BA, Miller A, Sercarz E."	6437975	2 - 6 months	both	25-Apr	(those with multiple values are bimodal)	<1 -9	 ( C3H.SW)<1 - 4; 30 -52			<1 -20			<1; 10 - 250	<1 -25	<1 -130	14-Jun			
Secondary anti - HUL responses in H-2 Ri mice	Score	Selective reversal of H-2 linked genetic unresponsiveness to lysozymes. I. Non-H-2 gene(s) closely linked to the Ir-2 locus on chromosome 2 permit(s) an antilysozyme response in H-2b mice.	"Genes outside of the mouse major histocompatibility complex (H-2) were found to be capable of specifically reversing the previously described nonresponsiveness to hen egg-white lysozyme (HEL) owing to H-2b immune response (Ir) genes. C3H.SW, BALB.B, and C57L, all of the H-2b haplotype, showed responsiveness to HEL, but not to human lysozyme (HUL). Mapping of the reversing gene(s) was attempted by testing H-2b recombinant inbred (RI) strains of mice carrying C3H, BALB, and C57L non-H-2 genes. Analysis of the strain distribution pattern of responsiveness with both CXB and BXH RI strains was consistent with the location of the responsible site within the H-3 region on chromosome 2. The anti-HEL proliferative responsiveness in two H-3 congenic strains of mice, B10.C(28NX)SN and B10.C-H-3cH-3a, that have BALB/c genes within the H-3 region confirmed the mapping, as well as localized the reversing gene(s) near the Ir-2 gene. The data are discussed with regard to the site of expression of the reversing gene(s) and its mechanism of action."	Immunogenetics	1984		"Sadegh-Nasseri S, Kipp DE, Taylor BA, Miller A, Sercarz E."	6437975	2 - 6 months	both	25-Apr	(those with multiple values are bimodal)<5 = 0;  6 - 25 = +/-;  26 - 125 = +;  126 - 625 = ++	0	 ( C3H.SW)0; +			0			0; +	0	+/-	+/-			
Distribution of Hba-a4 alleles in recombinant inbred strains	Locus:  Hba-a4	The alpha-globin pseudogene on mouse chromosome 17 is closely linked to H-2.	"DNA sequences homologous to adult alpha-globin genes are dispersed in the mouse. Two functional genes are tightly linked on chromosome 11. Pseudogenes have been assigned to chromosomes 15 and 17 by analysis of interspecies somatic cell hybrids. We have now further characterized the second of these pseudogenes, Hba-a4. The gene is highly polymorphic, with three forms occurring in a panel of 15 inbred strains and a fourth occurring in an inbred strain derived from M. m. molossinus. Analysis of Hba-a4 alleles in CXB, BXH, and AKXL recombinant inbred strains placed Hba-a4 6.60 +/- 3.14 cM centromeric to H-2. Analysis of congenic mouse strains confirmed the linkage and the gene order. Hba-a4 is the first mammalian dispersed pseudogene to be localized in a linkage map, and should provide a useful marker for the region of chromosome 17 proximal to H-2."	J Exp Med	1984	Mar	"D'Eustachio P, Fein B, Michaelson J, Taylor BA."	6321630							a	a	b	a	a	b	a	b	a	a	a	b
Distribution of Hba-a4 alleles in recombinant inbred strains	H-2	The alpha-globin pseudogene on mouse chromosome 17 is closely linked to H-2.	"DNA sequences homologous to adult alpha-globin genes are dispersed in the mouse. Two functional genes are tightly linked on chromosome 11. Pseudogenes have been assigned to chromosomes 15 and 17 by analysis of interspecies somatic cell hybrids. We have now further characterized the second of these pseudogenes, Hba-a4. The gene is highly polymorphic, with three forms occurring in a panel of 15 inbred strains and a fourth occurring in an inbred strain derived from M. m. molossinus. Analysis of Hba-a4 alleles in CXB, BXH, and AKXL recombinant inbred strains placed Hba-a4 6.60 +/- 3.14 cM centromeric to H-2. Analysis of congenic mouse strains confirmed the linkage and the gene order. Hba-a4 is the first mammalian dispersed pseudogene to be localized in a linkage map, and should provide a useful marker for the region of chromosome 17 proximal to H-2."	J Exp Med	1984	Mar	"D'Eustachio P, Fein B, Michaelson J, Taylor BA."	6321630							k	k	b	k	k	b	b	b	b	k	k	b
Distribution of Hba-a4 alleles in recombinant inbred strains	Upg-1	The alpha-globin pseudogene on mouse chromosome 17 is closely linked to H-2.	"DNA sequences homologous to adult alpha-globin genes are dispersed in the mouse. Two functional genes are tightly linked on chromosome 11. Pseudogenes have been assigned to chromosomes 15 and 17 by analysis of interspecies somatic cell hybrids. We have now further characterized the second of these pseudogenes, Hba-a4. The gene is highly polymorphic, with three forms occurring in a panel of 15 inbred strains and a fourth occurring in an inbred strain derived from M. m. molossinus. Analysis of Hba-a4 alleles in CXB, BXH, and AKXL recombinant inbred strains placed Hba-a4 6.60 +/- 3.14 cM centromeric to H-2. Analysis of congenic mouse strains confirmed the linkage and the gene order. Hba-a4 is the first mammalian dispersed pseudogene to be localized in a linkage map, and should provide a useful marker for the region of chromosome 17 proximal to H-2."	J Exp Med	1984	Mar	"D'Eustachio P, Fein B, Michaelson J, Taylor BA."	6321630							s	f	s	f	f	s	s	s	s	f	f	s
Footpad reaction and multiplication of bacilli in the popliteal lymph node	Footpad response:  Max. f. resp. in mm 	H-2-linked gene(s) influence the granulomatous reaction to viable Mycobacterium lepraemurium in the mouse.	"The genetic control of the granulomatous response to viable Mycobacterium lepraemurium (MLM) was studied in C3H and C57BL/6 inbred strains, BXH recombinant inbred strains, (C3H X C57BL) F1 hybrids, and backcross mice. The results indicate that an autosomal dominant gene, or linked complex of genes, has a marked influence on the footpad reaction to viable MLM. The distribution of responders and non-responders among 12 BXH recombinant inbred strains and linkage analysis in C3H X (C3H X C57BL)F1 backcross mice indicated that the response gene(s) are linked to the H-2 complex on chromosome 17. The same gene(s) also influence host restriction of MLM multiplication and thus appear to be the first H-2-linked gene(s) influencing resistance to a bacterial infection."	Scand J Immunol	1983	July	"Closs O, Lovik M, Wigzell H, Taylor BA."	6348937				mean	0.33	0.05	0.02	0.03	0.23	0.05	0.03	0.3	0.32	0.36	0.27	0.08	0.09	0.09
Footpad reaction and multiplication of bacilli in the popliteal lymph node	Footpad response:  Proportion of mice with Max. f. resp. >0.15 mm	H-2-linked gene(s) influence the granulomatous reaction to viable Mycobacterium lepraemurium in the mouse.	"The genetic control of the granulomatous response to viable Mycobacterium lepraemurium (MLM) was studied in C3H and C57BL/6 inbred strains, BXH recombinant inbred strains, (C3H X C57BL) F1 hybrids, and backcross mice. The results indicate that an autosomal dominant gene, or linked complex of genes, has a marked influence on the footpad reaction to viable MLM. The distribution of responders and non-responders among 12 BXH recombinant inbred strains and linkage analysis in C3H X (C3H X C57BL)F1 backcross mice indicated that the response gene(s) are linked to the H-2 complex on chromosome 17. The same gene(s) also influence host restriction of MLM multiplication and thus appear to be the first H-2-linked gene(s) influencing resistance to a bacterial infection."	Scand J Immunol	1983	July	"Closs O, Lovik M, Wigzell H, Taylor BA."	6348937					19/20	20-Jan	0/4	0/3	15/17	0/7	0/5	11-Sep	10-Oct	7-Jul	10-Sep	0/4	20-Apr	4-Feb
Footpad reaction and multiplication of bacilli in the popliteal lymph node	Footpad response:  Classification of strain	H-2-linked gene(s) influence the granulomatous reaction to viable Mycobacterium lepraemurium in the mouse.	"The genetic control of the granulomatous response to viable Mycobacterium lepraemurium (MLM) was studied in C3H and C57BL/6 inbred strains, BXH recombinant inbred strains, (C3H X C57BL) F1 hybrids, and backcross mice. The results indicate that an autosomal dominant gene, or linked complex of genes, has a marked influence on the footpad reaction to viable MLM. The distribution of responders and non-responders among 12 BXH recombinant inbred strains and linkage analysis in C3H X (C3H X C57BL)F1 backcross mice indicated that the response gene(s) are linked to the H-2 complex on chromosome 17. The same gene(s) also influence host restriction of MLM multiplication and thus appear to be the first H-2-linked gene(s) influencing resistance to a bacterial infection."	Scand J Immunol	1983	July	"Closs O, Lovik M, Wigzell H, Taylor BA."	6348937				R= responder; NR= nonresponder; I= intermediate	R	NR	NR	NR	R	NR	NR	R	R	R	R	NR	NR	I
Footpad reaction and multiplication of bacilli in the popliteal lymph node	No. of AFBx10^-6 om pop. 1. n.	H-2-linked gene(s) influence the granulomatous reaction to viable Mycobacterium lepraemurium in the mouse.	"The genetic control of the granulomatous response to viable Mycobacterium lepraemurium (MLM) was studied in C3H and C57BL/6 inbred strains, BXH recombinant inbred strains, (C3H X C57BL) F1 hybrids, and backcross mice. The results indicate that an autosomal dominant gene, or linked complex of genes, has a marked influence on the footpad reaction to viable MLM. The distribution of responders and non-responders among 12 BXH recombinant inbred strains and linkage analysis in C3H X (C3H X C57BL)F1 backcross mice indicated that the response gene(s) are linked to the H-2 complex on chromosome 17. The same gene(s) also influence host restriction of MLM multiplication and thus appear to be the first H-2-linked gene(s) influencing resistance to a bacterial infection."	Scand J Immunol	1983	July	"Closs O, Lovik M, Wigzell H, Taylor BA."	6348937					0.9	13		200	5.7	2.5	26	2.3	1.3	0.6	1.4	12	5.5	2.8
Footpad reaction and multiplication of bacilli in the popliteal lymph node	Phenotypic marker:    H-2	H-2-linked gene(s) influence the granulomatous reaction to viable Mycobacterium lepraemurium in the mouse.	"The genetic control of the granulomatous response to viable Mycobacterium lepraemurium (MLM) was studied in C3H and C57BL/6 inbred strains, BXH recombinant inbred strains, (C3H X C57BL) F1 hybrids, and backcross mice. The results indicate that an autosomal dominant gene, or linked complex of genes, has a marked influence on the footpad reaction to viable MLM. The distribution of responders and non-responders among 12 BXH recombinant inbred strains and linkage analysis in C3H X (C3H X C57BL)F1 backcross mice indicated that the response gene(s) are linked to the H-2 complex on chromosome 17. The same gene(s) also influence host restriction of MLM multiplication and thus appear to be the first H-2-linked gene(s) influencing resistance to a bacterial infection."	Scand J Immunol	1983	July	"Closs O, Lovik M, Wigzell H, Taylor BA."	6348937					b	k	k	k	b	k	k	b	b	b	b	k	k	b
Footpad reaction and multiplication of bacilli in the popliteal lymph node	Phenotypic marker: Igh-1	H-2-linked gene(s) influence the granulomatous reaction to viable Mycobacterium lepraemurium in the mouse.	"The genetic control of the granulomatous response to viable Mycobacterium lepraemurium (MLM) was studied in C3H and C57BL/6 inbred strains, BXH recombinant inbred strains, (C3H X C57BL) F1 hybrids, and backcross mice. The results indicate that an autosomal dominant gene, or linked complex of genes, has a marked influence on the footpad reaction to viable MLM. The distribution of responders and non-responders among 12 BXH recombinant inbred strains and linkage analysis in C3H X (C3H X C57BL)F1 backcross mice indicated that the response gene(s) are linked to the H-2 complex on chromosome 17. The same gene(s) also influence host restriction of MLM multiplication and thus appear to be the first H-2-linked gene(s) influencing resistance to a bacterial infection."	Scand J Immunol	1983	July	"Closs O, Lovik M, Wigzell H, Taylor BA."	6348937					b	j	j	b	j	j	j	b	j	b	b	j	b	j
Footpad reaction and multiplication of bacilli in the popliteal lymph node	Phenotypic marker:  Lsh	H-2-linked gene(s) influence the granulomatous reaction to viable Mycobacterium lepraemurium in the mouse.	"The genetic control of the granulomatous response to viable Mycobacterium lepraemurium (MLM) was studied in C3H and C57BL/6 inbred strains, BXH recombinant inbred strains, (C3H X C57BL) F1 hybrids, and backcross mice. The results indicate that an autosomal dominant gene, or linked complex of genes, has a marked influence on the footpad reaction to viable MLM. The distribution of responders and non-responders among 12 BXH recombinant inbred strains and linkage analysis in C3H X (C3H X C57BL)F1 backcross mice indicated that the response gene(s) are linked to the H-2 complex on chromosome 17. The same gene(s) also influence host restriction of MLM multiplication and thus appear to be the first H-2-linked gene(s) influencing resistance to a bacterial infection."	Scand J Immunol	1983	July	"Closs O, Lovik M, Wigzell H, Taylor BA."	6348937					s	r	r	s	r	r	r	r	r	s	s	s	r	r
Footpad reaction and multiplication of bacilli in the popliteal lymph node	Phenotypic marker:  Bcg	H-2-linked gene(s) influence the granulomatous reaction to viable Mycobacterium lepraemurium in the mouse.	"The genetic control of the granulomatous response to viable Mycobacterium lepraemurium (MLM) was studied in C3H and C57BL/6 inbred strains, BXH recombinant inbred strains, (C3H X C57BL) F1 hybrids, and backcross mice. The results indicate that an autosomal dominant gene, or linked complex of genes, has a marked influence on the footpad reaction to viable MLM. The distribution of responders and non-responders among 12 BXH recombinant inbred strains and linkage analysis in C3H X (C3H X C57BL)F1 backcross mice indicated that the response gene(s) are linked to the H-2 complex on chromosome 17. The same gene(s) also influence host restriction of MLM multiplication and thus appear to be the first H-2-linked gene(s) influencing resistance to a bacterial infection."	Scand J Immunol	1983	July	"Closs O, Lovik M, Wigzell H, Taylor BA."	6348937					s	r	r	s	r	r	r	r	r	s	s	s	r	r
Footpad reaction and multiplication of bacilli in the popliteal lymph node	Phenotypic marker:  Lps	H-2-linked gene(s) influence the granulomatous reaction to viable Mycobacterium lepraemurium in the mouse.	"The genetic control of the granulomatous response to viable Mycobacterium lepraemurium (MLM) was studied in C3H and C57BL/6 inbred strains, BXH recombinant inbred strains, (C3H X C57BL) F1 hybrids, and backcross mice. The results indicate that an autosomal dominant gene, or linked complex of genes, has a marked influence on the footpad reaction to viable MLM. The distribution of responders and non-responders among 12 BXH recombinant inbred strains and linkage analysis in C3H X (C3H X C57BL)F1 backcross mice indicated that the response gene(s) are linked to the H-2 complex on chromosome 17. The same gene(s) also influence host restriction of MLM multiplication and thus appear to be the first H-2-linked gene(s) influencing resistance to a bacterial infection."	Scand J Immunol	1983	July	"Closs O, Lovik M, Wigzell H, Taylor BA."	6348937					n	d	d	d	d	d	d	d	d	n	n	d	n	n
Number of ecotropic MuLV sequences in normal and infected BXH mice	No. of virus-specific sequences:  Spleen	Spontaneous and induced leukemias of myeloid origin in recombinant inbred BXH mice.	"BXH-2 recombinant inbred (RI) mice produce high titers of B-ecotropic murine leukemia virus beginning early in life and have a high incidence of non-T-cell leukemias that occur before 1 year of age. The leukemias that develop are in some cases associated with hind limb paralysis. In addition, a dualtropic mink cell focus-forming virus has been isolated from leukemic cells of BXH-2 mice. Immunological and cytochemical characterization of the BXH-2 leukemias showed that they are of the myeloid lineage. To assess the oncogenicity of the BXH-2 viruses, newborn mice of several BXH RI strains were inoculated at birth with biologically cloned B-ecotropic or mink cell focus-forming murine leukemia virus. These studies demonstrated that the B-ecotropic virus can induce myeloid leukemias in other BXH RI strains, whereas the dualtropic mink cell focus-forming isolates were nononcogenic in the strains tested. DNA-DNA reassociation analysis indicated that the organotropism of the B-ecotropic murine leukemia virus is confined to lymphoid tissues. Southern analysis of tumor DNAs showed that there was amplification of ecotropic virus-specific sequences in BXH-2 myeloid tumors and in all leukemias induced in other BXH RI strains by inoculation of the BXH-2 B-ecotropic virus. Although B-ecotropic virus is expressed in central nervous tissues of paralyzed BXH-2 mice, we were unable to induce the disorder in several BXH RI strains inoculated intracranially at birth with either the B-ecotropic or dualtropic virus. These results suggest that the paralysis that occurs in BXH-2 mice is due to the infiltration of leukemic cells into the central nervous system."	J Virol	1984	Sept	"Bedigian HG, Johnson DA, Jenkins NA, Copeland NG, Evans R."	6088784			4-Feb	normal - infected (average of three  independent kinetic analyses)							0.2 -1.3						1.4 - 2.3	
Number of ecotropic MuLV sequences in normal and infected BXH mice	No. of virus-specific sequences:  Bone Marrow  	Spontaneous and induced leukemias of myeloid origin in recombinant inbred BXH mice.	"BXH-2 recombinant inbred (RI) mice produce high titers of B-ecotropic murine leukemia virus beginning early in life and have a high incidence of non-T-cell leukemias that occur before 1 year of age. The leukemias that develop are in some cases associated with hind limb paralysis. In addition, a dualtropic mink cell focus-forming virus has been isolated from leukemic cells of BXH-2 mice. Immunological and cytochemical characterization of the BXH-2 leukemias showed that they are of the myeloid lineage. To assess the oncogenicity of the BXH-2 viruses, newborn mice of several BXH RI strains were inoculated at birth with biologically cloned B-ecotropic or mink cell focus-forming murine leukemia virus. These studies demonstrated that the B-ecotropic virus can induce myeloid leukemias in other BXH RI strains, whereas the dualtropic mink cell focus-forming isolates were nononcogenic in the strains tested. DNA-DNA reassociation analysis indicated that the organotropism of the B-ecotropic murine leukemia virus is confined to lymphoid tissues. Southern analysis of tumor DNAs showed that there was amplification of ecotropic virus-specific sequences in BXH-2 myeloid tumors and in all leukemias induced in other BXH RI strains by inoculation of the BXH-2 B-ecotropic virus. Although B-ecotropic virus is expressed in central nervous tissues of paralyzed BXH-2 mice, we were unable to induce the disorder in several BXH RI strains inoculated intracranially at birth with either the B-ecotropic or dualtropic virus. These results suggest that the paralysis that occurs in BXH-2 mice is due to the infiltration of leukemic cells into the central nervous system."	J Virol	1984	Sept	"Bedigian HG, Johnson DA, Jenkins NA, Copeland NG, Evans R."	6088784			4-Feb	normal - infected(average of three  independent kinetic analyses)							0.1 - 1.8						1.3 - 2.8	
Number of ecotropic MuLV sequences in normal and infected BXH mice	No. of virus-specific sequences:  Liver 	Spontaneous and induced leukemias of myeloid origin in recombinant inbred BXH mice.	"BXH-2 recombinant inbred (RI) mice produce high titers of B-ecotropic murine leukemia virus beginning early in life and have a high incidence of non-T-cell leukemias that occur before 1 year of age. The leukemias that develop are in some cases associated with hind limb paralysis. In addition, a dualtropic mink cell focus-forming virus has been isolated from leukemic cells of BXH-2 mice. Immunological and cytochemical characterization of the BXH-2 leukemias showed that they are of the myeloid lineage. To assess the oncogenicity of the BXH-2 viruses, newborn mice of several BXH RI strains were inoculated at birth with biologically cloned B-ecotropic or mink cell focus-forming murine leukemia virus. These studies demonstrated that the B-ecotropic virus can induce myeloid leukemias in other BXH RI strains, whereas the dualtropic mink cell focus-forming isolates were nononcogenic in the strains tested. DNA-DNA reassociation analysis indicated that the organotropism of the B-ecotropic murine leukemia virus is confined to lymphoid tissues. Southern analysis of tumor DNAs showed that there was amplification of ecotropic virus-specific sequences in BXH-2 myeloid tumors and in all leukemias induced in other BXH RI strains by inoculation of the BXH-2 B-ecotropic virus. Although B-ecotropic virus is expressed in central nervous tissues of paralyzed BXH-2 mice, we were unable to induce the disorder in several BXH RI strains inoculated intracranially at birth with either the B-ecotropic or dualtropic virus. These results suggest that the paralysis that occurs in BXH-2 mice is due to the infiltration of leukemic cells into the central nervous system."	J Virol	1984	Sept	"Bedigian HG, Johnson DA, Jenkins NA, Copeland NG, Evans R."	6088784			4-Feb	normal - infected(average of three  independent kinetic analyses)							not determined - 0.1						1.3 - 1.4	
Number of ecotropic MuLV sequences in normal and infected BXH mice	No. of virus-specific sequences:  Thymus	Spontaneous and induced leukemias of myeloid origin in recombinant inbred BXH mice.	"BXH-2 recombinant inbred (RI) mice produce high titers of B-ecotropic murine leukemia virus beginning early in life and have a high incidence of non-T-cell leukemias that occur before 1 year of age. The leukemias that develop are in some cases associated with hind limb paralysis. In addition, a dualtropic mink cell focus-forming virus has been isolated from leukemic cells of BXH-2 mice. Immunological and cytochemical characterization of the BXH-2 leukemias showed that they are of the myeloid lineage. To assess the oncogenicity of the BXH-2 viruses, newborn mice of several BXH RI strains were inoculated at birth with biologically cloned B-ecotropic or mink cell focus-forming murine leukemia virus. These studies demonstrated that the B-ecotropic virus can induce myeloid leukemias in other BXH RI strains, whereas the dualtropic mink cell focus-forming isolates were nononcogenic in the strains tested. DNA-DNA reassociation analysis indicated that the organotropism of the B-ecotropic murine leukemia virus is confined to lymphoid tissues. Southern analysis of tumor DNAs showed that there was amplification of ecotropic virus-specific sequences in BXH-2 myeloid tumors and in all leukemias induced in other BXH RI strains by inoculation of the BXH-2 B-ecotropic virus. Although B-ecotropic virus is expressed in central nervous tissues of paralyzed BXH-2 mice, we were unable to induce the disorder in several BXH RI strains inoculated intracranially at birth with either the B-ecotropic or dualtropic virus. These results suggest that the paralysis that occurs in BXH-2 mice is due to the infiltration of leukemic cells into the central nervous system."	J Virol	1984	Sept	"Bedigian HG, Johnson DA, Jenkins NA, Copeland NG, Evans R."	6088784			4-Feb	normal - infected(average of three  independent kinetic analyses)							0.1 - 0.1						1.4 - 1.5	
Number of ecotropic MuLV sequences in normal and infected BXH mice	No. of virus-specific sequences:  Brain	Spontaneous and induced leukemias of myeloid origin in recombinant inbred BXH mice.	"BXH-2 recombinant inbred (RI) mice produce high titers of B-ecotropic murine leukemia virus beginning early in life and have a high incidence of non-T-cell leukemias that occur before 1 year of age. The leukemias that develop are in some cases associated with hind limb paralysis. In addition, a dualtropic mink cell focus-forming virus has been isolated from leukemic cells of BXH-2 mice. Immunological and cytochemical characterization of the BXH-2 leukemias showed that they are of the myeloid lineage. To assess the oncogenicity of the BXH-2 viruses, newborn mice of several BXH RI strains were inoculated at birth with biologically cloned B-ecotropic or mink cell focus-forming murine leukemia virus. These studies demonstrated that the B-ecotropic virus can induce myeloid leukemias in other BXH RI strains, whereas the dualtropic mink cell focus-forming isolates were nononcogenic in the strains tested. DNA-DNA reassociation analysis indicated that the organotropism of the B-ecotropic murine leukemia virus is confined to lymphoid tissues. Southern analysis of tumor DNAs showed that there was amplification of ecotropic virus-specific sequences in BXH-2 myeloid tumors and in all leukemias induced in other BXH RI strains by inoculation of the BXH-2 B-ecotropic virus. Although B-ecotropic virus is expressed in central nervous tissues of paralyzed BXH-2 mice, we were unable to induce the disorder in several BXH RI strains inoculated intracranially at birth with either the B-ecotropic or dualtropic virus. These results suggest that the paralysis that occurs in BXH-2 mice is due to the infiltration of leukemic cells into the central nervous system."	J Virol	1984	Sept	"Bedigian HG, Johnson DA, Jenkins NA, Copeland NG, Evans R."	6088784			4-Feb	normal - infected(average of three  independent kinetic analyses)							not determined - 0.1						1.3 - 1.4	
"Inheritance of Es-1, Pgm-1, and Fv-2 alleles and ecotopric MuLV DNA  sequences in BXH RI strains"	Blv	Ecotropic murine leukemia virus DNA content of normal and lymphomatous tissues of BXH-2 recombinant inbred mice.	"BXH-2 recombinant inbred mice spontaneously produce a B-tropic murine leukemia virus (MuLV) beginning early in life and have a high incidence of non-T-cell lymphomas. These traits are not characteristic of the progenitor strains (C57BL/6J and C3H/HeJ) or of 11 other BXH recombinant inbred strains. Since B-tropic virus expression may be causally related to the high incidence of lymphoma in this strain, we have analyzed the ecotropic MuLV DNA content of both normal and lymphomatous tissues of BXH-2 mice. Southern analysis and hybridization with an ecotropic MuLV DNA-specific probe showed that DNA of normal BXH-2 tissues contained both parental N-tropic MuLV proviruses but lacked endogenous B-tropic MuLV DNA sequences. In addition, none of 116 F1 hybrid mice derived from male BXH-2 mice spontaneously produced ecotropic MuLV early in life. These results suggest that the B-tropic virus is horizontally transmitted in BXH-2 mice. Southern analysis of DNA from tumor tissues of 12 BXH-2 mice showed that amplification of ecotropic-specific DNA sequences had occurred in lymphomatous tissues of 3 mice and suggested that these tumors were monoclonal. The number of newly acquired proviruses, which appeared to be structurally nondefective and integrated at different sites, varied from one to three copies. Since lymphomatous tissues from only 3 of 12 mice examined carried additional detectable ecotropic proviruses, these results suggest that amplification of ecotropic MuLV DNA sequences is not required for maintenance of transformation in BXH-2 lymphomas."	J Virol	1982	May	"Jenkins NA, Copeland NG, Taylor BA, Bedigian HG, Lee BK."	6283161				B = C57BL/6J; H =C3H/HeJ			B	B	H	H	H	H	B	B	B	B	B	B
"Inheritance of Es-1, Pgm-1, and Fv-2 alleles and ecotopric MuLV DNA  sequences in BXH RI strains"	Es-1	Ecotropic murine leukemia virus DNA content of normal and lymphomatous tissues of BXH-2 recombinant inbred mice.	"BXH-2 recombinant inbred mice spontaneously produce a B-tropic murine leukemia virus (MuLV) beginning early in life and have a high incidence of non-T-cell lymphomas. These traits are not characteristic of the progenitor strains (C57BL/6J and C3H/HeJ) or of 11 other BXH recombinant inbred strains. Since B-tropic virus expression may be causally related to the high incidence of lymphoma in this strain, we have analyzed the ecotropic MuLV DNA content of both normal and lymphomatous tissues of BXH-2 mice. Southern analysis and hybridization with an ecotropic MuLV DNA-specific probe showed that DNA of normal BXH-2 tissues contained both parental N-tropic MuLV proviruses but lacked endogenous B-tropic MuLV DNA sequences. In addition, none of 116 F1 hybrid mice derived from male BXH-2 mice spontaneously produced ecotropic MuLV early in life. These results suggest that the B-tropic virus is horizontally transmitted in BXH-2 mice. Southern analysis of DNA from tumor tissues of 12 BXH-2 mice showed that amplification of ecotropic-specific DNA sequences had occurred in lymphomatous tissues of 3 mice and suggested that these tumors were monoclonal. The number of newly acquired proviruses, which appeared to be structurally nondefective and integrated at different sites, varied from one to three copies. Since lymphomatous tissues from only 3 of 12 mice examined carried additional detectable ecotropic proviruses, these results suggest that amplification of ecotropic MuLV DNA sequences is not required for maintenance of transformation in BXH-2 lymphomas."	J Virol	1982	May	"Jenkins NA, Copeland NG, Taylor BA, Bedigian HG, Lee BK."	6283161				B = C57BL/6J; H =C3H/HeJ			B	H	H	B	B	B	B	B	B	H	B	H
"Inheritance of Es-1, Pgm-1, and Fv-2 alleles and ecotopric MuLV DNA  sequences in BXH RI strains"	Pgm-1	Ecotropic murine leukemia virus DNA content of normal and lymphomatous tissues of BXH-2 recombinant inbred mice.	"BXH-2 recombinant inbred mice spontaneously produce a B-tropic murine leukemia virus (MuLV) beginning early in life and have a high incidence of non-T-cell lymphomas. These traits are not characteristic of the progenitor strains (C57BL/6J and C3H/HeJ) or of 11 other BXH recombinant inbred strains. Since B-tropic virus expression may be causally related to the high incidence of lymphoma in this strain, we have analyzed the ecotropic MuLV DNA content of both normal and lymphomatous tissues of BXH-2 mice. Southern analysis and hybridization with an ecotropic MuLV DNA-specific probe showed that DNA of normal BXH-2 tissues contained both parental N-tropic MuLV proviruses but lacked endogenous B-tropic MuLV DNA sequences. In addition, none of 116 F1 hybrid mice derived from male BXH-2 mice spontaneously produced ecotropic MuLV early in life. These results suggest that the B-tropic virus is horizontally transmitted in BXH-2 mice. Southern analysis of DNA from tumor tissues of 12 BXH-2 mice showed that amplification of ecotropic-specific DNA sequences had occurred in lymphomatous tissues of 3 mice and suggested that these tumors were monoclonal. The number of newly acquired proviruses, which appeared to be structurally nondefective and integrated at different sites, varied from one to three copies. Since lymphomatous tissues from only 3 of 12 mice examined carried additional detectable ecotropic proviruses, these results suggest that amplification of ecotropic MuLV DNA sequences is not required for maintenance of transformation in BXH-2 lymphomas."	J Virol	1982	May	"Jenkins NA, Copeland NG, Taylor BA, Bedigian HG, Lee BK."	6283161				B = C57BL/6J; H =C3H/HeJ			H	H	H	B	B	H	H	B	B	B	H	H
"Inheritance of Es-1, Pgm-1, and Fv-2 alleles and ecotopric MuLV DNA  sequences in BXH RI strains"	C3v	Ecotropic murine leukemia virus DNA content of normal and lymphomatous tissues of BXH-2 recombinant inbred mice.	"BXH-2 recombinant inbred mice spontaneously produce a B-tropic murine leukemia virus (MuLV) beginning early in life and have a high incidence of non-T-cell lymphomas. These traits are not characteristic of the progenitor strains (C57BL/6J and C3H/HeJ) or of 11 other BXH recombinant inbred strains. Since B-tropic virus expression may be causally related to the high incidence of lymphoma in this strain, we have analyzed the ecotropic MuLV DNA content of both normal and lymphomatous tissues of BXH-2 mice. Southern analysis and hybridization with an ecotropic MuLV DNA-specific probe showed that DNA of normal BXH-2 tissues contained both parental N-tropic MuLV proviruses but lacked endogenous B-tropic MuLV DNA sequences. In addition, none of 116 F1 hybrid mice derived from male BXH-2 mice spontaneously produced ecotropic MuLV early in life. These results suggest that the B-tropic virus is horizontally transmitted in BXH-2 mice. Southern analysis of DNA from tumor tissues of 12 BXH-2 mice showed that amplification of ecotropic-specific DNA sequences had occurred in lymphomatous tissues of 3 mice and suggested that these tumors were monoclonal. The number of newly acquired proviruses, which appeared to be structurally nondefective and integrated at different sites, varied from one to three copies. Since lymphomatous tissues from only 3 of 12 mice examined carried additional detectable ecotropic proviruses, these results suggest that amplification of ecotropic MuLV DNA sequences is not required for maintenance of transformation in BXH-2 lymphomas."	J Virol	1982	May	"Jenkins NA, Copeland NG, Taylor BA, Bedigian HG, Lee BK."	6283161				B = C57BL/6J; H =C3H/HeJ			H	H	B	H	B	H	H	B	B	H	B	H
"Inheritance of Es-1, Pgm-1, and Fv-2 alleles and ecotopric MuLV DNA  sequences in BXH RI strains"	Fv-2	Ecotropic murine leukemia virus DNA content of normal and lymphomatous tissues of BXH-2 recombinant inbred mice.	"BXH-2 recombinant inbred mice spontaneously produce a B-tropic murine leukemia virus (MuLV) beginning early in life and have a high incidence of non-T-cell lymphomas. These traits are not characteristic of the progenitor strains (C57BL/6J and C3H/HeJ) or of 11 other BXH recombinant inbred strains. Since B-tropic virus expression may be causally related to the high incidence of lymphoma in this strain, we have analyzed the ecotropic MuLV DNA content of both normal and lymphomatous tissues of BXH-2 mice. Southern analysis and hybridization with an ecotropic MuLV DNA-specific probe showed that DNA of normal BXH-2 tissues contained both parental N-tropic MuLV proviruses but lacked endogenous B-tropic MuLV DNA sequences. In addition, none of 116 F1 hybrid mice derived from male BXH-2 mice spontaneously produced ecotropic MuLV early in life. These results suggest that the B-tropic virus is horizontally transmitted in BXH-2 mice. Southern analysis of DNA from tumor tissues of 12 BXH-2 mice showed that amplification of ecotropic-specific DNA sequences had occurred in lymphomatous tissues of 3 mice and suggested that these tumors were monoclonal. The number of newly acquired proviruses, which appeared to be structurally nondefective and integrated at different sites, varied from one to three copies. Since lymphomatous tissues from only 3 of 12 mice examined carried additional detectable ecotropic proviruses, these results suggest that amplification of ecotropic MuLV DNA sequences is not required for maintenance of transformation in BXH-2 lymphomas."	J Virol	1982	May	"Jenkins NA, Copeland NG, Taylor BA, Bedigian HG, Lee BK."	6283161				B = C57BL/6J; H =C3H/HeJ			H	H	B	H	B	H	H	B	B	H	B	H
Inc and Inb classification of BXH recombianat inbred strains	Crosses to BALB/c or C3H:  Mean syncytia per culture 	A locus that enhances the induction of endogenous ecotropic murine leukemia viruses is distinct from genome-length ecotropic proviruses.	"The segregation of genes that enhance the induction of ecotropic murine leukemia viruses (In loci) has been compared with the segregation of ecotropic-specific nucleotide sequences in 12 low-leukemic mouse strains and 18 recombinant inbred strains. Endogenous ecotropic viruses of these strains are of genome length and structurally similar to AKR ecotropic proviruses. Low-leukemic strains of related pedigree contain ecotropic proviruses at common integration sites. Loci previously identified which enhance induction of ecotropic viruses (In genes) were correlated with the inheritance of ecotropic viral sequences in inbred low-leukemic mouse strains and in CXB recombinant inbred mouse strains. However, four BXH recombinant inbred strains were observed to possess an In gene(s) yet lack the probed envelope gene region for the corresponding endogenous ecotropic virus. These observations indicate that at least one gene that enhances ecotropic virus expression in vitro is encoded by DNA sequences outside ecotropic proviruses or by subgenomic viral sequences."	J Virol	1982	Dec	"Horowitz JM, Risser R."	6294342				number of cultures examined after hyphen	15 -38	0 - 10		43 - 4	6-Jan	0 - 8	0 - 17	0 - 9	95 - 6	32 - 13	110 - 3	not determined	159 - 15	161 - 14
Inc and Inb classification of BXH recombianat inbred strains	Crosses to BALB/c or C3H:  Inb-1 genotype	A locus that enhances the induction of endogenous ecotropic murine leukemia viruses is distinct from genome-length ecotropic proviruses.	"The segregation of genes that enhance the induction of ecotropic murine leukemia viruses (In loci) has been compared with the segregation of ecotropic-specific nucleotide sequences in 12 low-leukemic mouse strains and 18 recombinant inbred strains. Endogenous ecotropic viruses of these strains are of genome length and structurally similar to AKR ecotropic proviruses. Low-leukemic strains of related pedigree contain ecotropic proviruses at common integration sites. Loci previously identified which enhance induction of ecotropic viruses (In genes) were correlated with the inheritance of ecotropic viral sequences in inbred low-leukemic mouse strains and in CXB recombinant inbred mouse strains. However, four BXH recombinant inbred strains were observed to possess an In gene(s) yet lack the probed envelope gene region for the corresponding endogenous ecotropic virus. These observations indicate that at least one gene that enhances ecotropic virus expression in vitro is encoded by DNA sequences outside ecotropic proviruses or by subgenomic viral sequences."	J Virol	1982	Dec	"Horowitz JM, Risser R."	6294342					+  	-		+	-	-	-	-	+	+	+		+	+
Inc and Inb classification of BXH recombianat inbred strains	Crosses to C57BL/6 mice:  Mean syncytia per culture 	A locus that enhances the induction of endogenous ecotropic murine leukemia viruses is distinct from genome-length ecotropic proviruses.	"The segregation of genes that enhance the induction of ecotropic murine leukemia viruses (In loci) has been compared with the segregation of ecotropic-specific nucleotide sequences in 12 low-leukemic mouse strains and 18 recombinant inbred strains. Endogenous ecotropic viruses of these strains are of genome length and structurally similar to AKR ecotropic proviruses. Low-leukemic strains of related pedigree contain ecotropic proviruses at common integration sites. Loci previously identified which enhance induction of ecotropic viruses (In genes) were correlated with the inheritance of ecotropic viral sequences in inbred low-leukemic mouse strains and in CXB recombinant inbred mouse strains. However, four BXH recombinant inbred strains were observed to possess an In gene(s) yet lack the probed envelope gene region for the corresponding endogenous ecotropic virus. These observations indicate that at least one gene that enhances ecotropic virus expression in vitro is encoded by DNA sequences outside ecotropic proviruses or by subgenomic viral sequences."	J Virol	1982	Dec	"Horowitz JM, Risser R."	6294342				number of cultures examined after hyphen	0.5 - 44	15 - 38		50 - 8	0 - 8	58 - 4	14 - 27	17 - 6	121 - 16	19-Jul	13-Nov	20 - 4	44 - 16	132 - 15
Inc and Inb classification of BXH recombianat inbred strains	Crosses to C57BL/6 mice: Inb-1 genotype	A locus that enhances the induction of endogenous ecotropic murine leukemia viruses is distinct from genome-length ecotropic proviruses.	"The segregation of genes that enhance the induction of ecotropic murine leukemia viruses (In loci) has been compared with the segregation of ecotropic-specific nucleotide sequences in 12 low-leukemic mouse strains and 18 recombinant inbred strains. Endogenous ecotropic viruses of these strains are of genome length and structurally similar to AKR ecotropic proviruses. Low-leukemic strains of related pedigree contain ecotropic proviruses at common integration sites. Loci previously identified which enhance induction of ecotropic viruses (In genes) were correlated with the inheritance of ecotropic viral sequences in inbred low-leukemic mouse strains and in CXB recombinant inbred mouse strains. However, four BXH recombinant inbred strains were observed to possess an In gene(s) yet lack the probed envelope gene region for the corresponding endogenous ecotropic virus. These observations indicate that at least one gene that enhances ecotropic virus expression in vitro is encoded by DNA sequences outside ecotropic proviruses or by subgenomic viral sequences."	J Virol	1982	Dec	"Horowitz JM, Risser R."	6294342					-	+		+	-	+	+	+	+	+	+	+	+	+
Responsiveness of BXH RI strains to microwave-induced increases in the frequency of splenic CRL	Percent CRL:  Microwave	Evidence for genetic control of microwave-induced augmentation of complement receptor-bearing B lymphocytes.	"The genetic control of 2450 MHz microwave-induced increase in complement receptor-bearing B lymphocytes (CRL) was studied using congenic, backcross, and recombinant inbred (RI) strains of mice. Mice were exposed to 2450 MHz microwaves (0.6 W; 10-14 W/kg) in an environmentally controlled waveguide and were assayed for CRL on days 3 or 6 post-exposure. Genetic studies of responder X nonresponder F1 mice and backcross analysis of nonresponder X (responder X nonresponder) F1 mice indicated that microwave susceptibility was controlled by a single, dominant Mendelian gene. Crosses between two nonresponder strains failed to restore the responder state. The dichotomy in microwave susceptibility between two strains congenic at the H-2--T1a region on chromosome 17 (AKR-responder and B.6-H-2k-nonresponder) indicated the noninvolvement of the Crl-1 gene and that the essential gene was located outside the H-2 region. This was confirmed by the responsiveness of the C3H-H-2o strain, which possesses a nonresponder H-2 haplotype and responder background genes. The strain distribution of microwave responsiveness in the BXH RI lines demonstrated that the microwave-induced increase in CRL was controlled by a single regulatory gene located on chromosome 5. We also analyzed the microwave responsiveness of two congenic strains of mice that possess different C3H/HeJ segments of chromosome 5 inserted into a C57BL/6J background. The JGBF/LeTy strain exhibited an increase in CRL indicating it possessed the segment of C3H/HeJ chromosome 5 that controls microwave responsiveness. The C57BL/6JTy-le strain remained nonresponsive. This places the essential regulatory gene to the right of the PgM-1 locus and to the left of the rd locus on chromosome 5."	J Immunol	1982	Oct	"Schlagel CJ, Ahmed A."	6980940				%			29	35.3	29.1	27.5	22.6	28.9	29.4	29.3		30.4	19.8	24.1
Responsiveness of BXH RI strains to microwave-induced increases in the frequency of splenic CRL	Percent CRL:Control	Evidence for genetic control of microwave-induced augmentation of complement receptor-bearing B lymphocytes.	"The genetic control of 2450 MHz microwave-induced increase in complement receptor-bearing B lymphocytes (CRL) was studied using congenic, backcross, and recombinant inbred (RI) strains of mice. Mice were exposed to 2450 MHz microwaves (0.6 W; 10-14 W/kg) in an environmentally controlled waveguide and were assayed for CRL on days 3 or 6 post-exposure. Genetic studies of responder X nonresponder F1 mice and backcross analysis of nonresponder X (responder X nonresponder) F1 mice indicated that microwave susceptibility was controlled by a single, dominant Mendelian gene. Crosses between two nonresponder strains failed to restore the responder state. The dichotomy in microwave susceptibility between two strains congenic at the H-2--T1a region on chromosome 17 (AKR-responder and B.6-H-2k-nonresponder) indicated the noninvolvement of the Crl-1 gene and that the essential gene was located outside the H-2 region. This was confirmed by the responsiveness of the C3H-H-2o strain, which possesses a nonresponder H-2 haplotype and responder background genes. The strain distribution of microwave responsiveness in the BXH RI lines demonstrated that the microwave-induced increase in CRL was controlled by a single regulatory gene located on chromosome 5. We also analyzed the microwave responsiveness of two congenic strains of mice that possess different C3H/HeJ segments of chromosome 5 inserted into a C57BL/6J background. The JGBF/LeTy strain exhibited an increase in CRL indicating it possessed the segment of C3H/HeJ chromosome 5 that controls microwave responsiveness. The C57BL/6JTy-le strain remained nonresponsive. This places the essential regulatory gene to the right of the PgM-1 locus and to the left of the rd locus on chromosome 5."	J Immunol	1982	Oct	"Schlagel CJ, Ahmed A."	6980940				%			27.9	24.3	22.4	30.2	24.4	22.2	22.4	16.7		20.5	22.6	17.9
Responsiveness of BXH RI strains to microwave-induced increases in the frequency of splenic CRL	Percent CRL:p	Evidence for genetic control of microwave-induced augmentation of complement receptor-bearing B lymphocytes.	"The genetic control of 2450 MHz microwave-induced increase in complement receptor-bearing B lymphocytes (CRL) was studied using congenic, backcross, and recombinant inbred (RI) strains of mice. Mice were exposed to 2450 MHz microwaves (0.6 W; 10-14 W/kg) in an environmentally controlled waveguide and were assayed for CRL on days 3 or 6 post-exposure. Genetic studies of responder X nonresponder F1 mice and backcross analysis of nonresponder X (responder X nonresponder) F1 mice indicated that microwave susceptibility was controlled by a single, dominant Mendelian gene. Crosses between two nonresponder strains failed to restore the responder state. The dichotomy in microwave susceptibility between two strains congenic at the H-2--T1a region on chromosome 17 (AKR-responder and B.6-H-2k-nonresponder) indicated the noninvolvement of the Crl-1 gene and that the essential gene was located outside the H-2 region. This was confirmed by the responsiveness of the C3H-H-2o strain, which possesses a nonresponder H-2 haplotype and responder background genes. The strain distribution of microwave responsiveness in the BXH RI lines demonstrated that the microwave-induced increase in CRL was controlled by a single regulatory gene located on chromosome 5. We also analyzed the microwave responsiveness of two congenic strains of mice that possess different C3H/HeJ segments of chromosome 5 inserted into a C57BL/6J background. The JGBF/LeTy strain exhibited an increase in CRL indicating it possessed the segment of C3H/HeJ chromosome 5 that controls microwave responsiveness. The C57BL/6JTy-le strain remained nonresponsive. This places the essential regulatory gene to the right of the PgM-1 locus and to the left of the rd locus on chromosome 5."	J Immunol	1982	Oct	"Schlagel CJ, Ahmed A."	6980940				%			not significant	<0.001	<0.05	not significant	not significant	<0.05	<0.001	<0.05		<0.1	not significant	<0.01
Inheritance of chromosome 5 marker Gus and susceptibility to 2450 MHz microwave-induced increases in CR spleen cells in BXH RI strains	Gus	Evidence for genetic control of microwave-induced augmentation of complement receptor-bearing B lymphocytes.	"The genetic control of 2450 MHz microwave-induced increase in complement receptor-bearing B lymphocytes (CRL) was studied using congenic, backcross, and recombinant inbred (RI) strains of mice. Mice were exposed to 2450 MHz microwaves (0.6 W; 10-14 W/kg) in an environmentally controlled waveguide and were assayed for CRL on days 3 or 6 post-exposure. Genetic studies of responder X nonresponder F1 mice and backcross analysis of nonresponder X (responder X nonresponder) F1 mice indicated that microwave susceptibility was controlled by a single, dominant Mendelian gene. Crosses between two nonresponder strains failed to restore the responder state. The dichotomy in microwave susceptibility between two strains congenic at the H-2--T1a region on chromosome 17 (AKR-responder and B.6-H-2k-nonresponder) indicated the noninvolvement of the Crl-1 gene and that the essential gene was located outside the H-2 region. This was confirmed by the responsiveness of the C3H-H-2o strain, which possesses a nonresponder H-2 haplotype and responder background genes. The strain distribution of microwave responsiveness in the BXH RI lines demonstrated that the microwave-induced increase in CRL was controlled by a single regulatory gene located on chromosome 5. We also analyzed the microwave responsiveness of two congenic strains of mice that possess different C3H/HeJ segments of chromosome 5 inserted into a C57BL/6J background. The JGBF/LeTy strain exhibited an increase in CRL indicating it possessed the segment of C3H/HeJ chromosome 5 that controls microwave responsiveness. The C57BL/6JTy-le strain remained nonresponsive. This places the essential regulatory gene to the right of the PgM-1 locus and to the left of the rd locus on chromosome 5."	J Immunol	1982	Oct	"Schlagel CJ, Ahmed A."	6980940				B = C57BL/6J; H =C3H/HeJ			B	H	H	B	B	H	H	H	B	B	B	H
Inheritance of chromosome 5 marker Gus and susceptibility to 2450 MHz microwave-induced increases in CR spleen cells in BXH RI strains	CRL	Evidence for genetic control of microwave-induced augmentation of complement receptor-bearing B lymphocytes.	"The genetic control of 2450 MHz microwave-induced increase in complement receptor-bearing B lymphocytes (CRL) was studied using congenic, backcross, and recombinant inbred (RI) strains of mice. Mice were exposed to 2450 MHz microwaves (0.6 W; 10-14 W/kg) in an environmentally controlled waveguide and were assayed for CRL on days 3 or 6 post-exposure. Genetic studies of responder X nonresponder F1 mice and backcross analysis of nonresponder X (responder X nonresponder) F1 mice indicated that microwave susceptibility was controlled by a single, dominant Mendelian gene. Crosses between two nonresponder strains failed to restore the responder state. The dichotomy in microwave susceptibility between two strains congenic at the H-2--T1a region on chromosome 17 (AKR-responder and B.6-H-2k-nonresponder) indicated the noninvolvement of the Crl-1 gene and that the essential gene was located outside the H-2 region. This was confirmed by the responsiveness of the C3H-H-2o strain, which possesses a nonresponder H-2 haplotype and responder background genes. The strain distribution of microwave responsiveness in the BXH RI lines demonstrated that the microwave-induced increase in CRL was controlled by a single regulatory gene located on chromosome 5. We also analyzed the microwave responsiveness of two congenic strains of mice that possess different C3H/HeJ segments of chromosome 5 inserted into a C57BL/6J background. The JGBF/LeTy strain exhibited an increase in CRL indicating it possessed the segment of C3H/HeJ chromosome 5 that controls microwave responsiveness. The C57BL/6JTy-le strain remained nonresponsive. This places the essential regulatory gene to the right of the PgM-1 locus and to the left of the rd locus on chromosome 5."	J Immunol	1982	Oct	"Schlagel CJ, Ahmed A."	6980940				B = C57BL/6J; H =C3H/HeJ			B	H	H	B	B	H	H	H		B	B	H
Segregation of Ly-m20 and Mls genes in BXH recombinant inbred strains	Ly-m20	A new mouse cell-surface antigen (Ly-m20) controlled by a gene linked to Mls locus and defined by monoclonal antibodies.	"Five monoclonal antibodies were established by the fusion of mouse myeloma cells (NS.1) with spleen cells from A and (A x C3H/An)F1 mice hyperimmunized with 70Z/3 tumor cells. These antibodies recognized a new antigenic specificity provisionally called Ly-m20.2. In direct cytotoxicity assays, 60 percent of cells in spleen, 40 percent in lymph node, 50 percent in bone marrow and less than 5 percent in thymus were found to react with three of the five antibodies, whereas the two others yielded somewhat lower cytotoxicity indices. The Ly-m20.2 antigen was also expressed on cells derived from liver and kidney but not on cells derived from brain. As judged from cytotoxicity assays with separated T and B cells, Ly-m20.2 antigen is carried preferentially on B lymphocytes. Direct plaque-forming cells (PFC) were completely eliminated by Ly-m20.2-specific antibody and complement. Linkage tests by analysis in 20 (CBA/J x C3H/An) x C3H/An backcross mice and by segregation analysis of BXH and SWXL recombinant inbred strains indicate close association of the loci controlling Ly-m20.2 and M1s antigens on chromosome 1."	Immunogenetics	1981		"Kimura S, Tada N, Nakayama E, Liu Y, Hammerling U."	6173319				B = C57BL/6J; H =C3H/HeJ				B	B	H	B	B	H		B	H	H	B
Segregation of Ly-m20 and Mls genes in BXH recombinant inbred strains	Mls	A new mouse cell-surface antigen (Ly-m20) controlled by a gene linked to Mls locus and defined by monoclonal antibodies.	"Five monoclonal antibodies were established by the fusion of mouse myeloma cells (NS.1) with spleen cells from A and (A x C3H/An)F1 mice hyperimmunized with 70Z/3 tumor cells. These antibodies recognized a new antigenic specificity provisionally called Ly-m20.2. In direct cytotoxicity assays, 60 percent of cells in spleen, 40 percent in lymph node, 50 percent in bone marrow and less than 5 percent in thymus were found to react with three of the five antibodies, whereas the two others yielded somewhat lower cytotoxicity indices. The Ly-m20.2 antigen was also expressed on cells derived from liver and kidney but not on cells derived from brain. As judged from cytotoxicity assays with separated T and B cells, Ly-m20.2 antigen is carried preferentially on B lymphocytes. Direct plaque-forming cells (PFC) were completely eliminated by Ly-m20.2-specific antibody and complement. Linkage tests by analysis in 20 (CBA/J x C3H/An) x C3H/An backcross mice and by segregation analysis of BXH and SWXL recombinant inbred strains indicate close association of the loci controlling Ly-m20.2 and M1s antigens on chromosome 1."	Immunogenetics	1981		"Kimura S, Tada N, Nakayama E, Liu Y, Hammerling U."	6173319				B = C57BL/6J; H =C3H/HeJ				B	B	H	B	B	H		B	H	H	B
Fv-1 and H-2 genotypes of BXH RI strains	Fv-1 genotype	Expression of murine leukemia viruses in the highly lymphomatous BXH-2 recombinant inbred mouse strain.	"Among 12 recombinant inbred strains of mice derived from crossing two strains, C57BL/6J and C3H/HeJ, which have a low incidence of neoplastic disease, one strain (BXH-2) has been found to have a high incidence of lymphoma, of non-T-cell origin, at an early age. The BXH-2 strain carries the Fv-1b allele and spontaneously expresses a B-tropic murine leukemia virus beginning at as early as 10 days of gestation and continuing throughout their life. No significant differences in ecotropic virus titers were observed at any age tested (16 to 17 days of gestation through 7 months), whereas xenotropic virus was first detected in lymphoid tissues of 2-month-old mice and virus titers increased with age. Dual tropic virus(es), which induced cytopathic changes on mink lung cells, was isolated from BXH-2 lymphomatous tissues. Unlike AKR mink lung focus-forming virus (N-tropic recombinant), BXH-2 dual tropic virus is B tropic and induces cytopathic changes in mouse fibroblast cultures as well. The BXH-2 mouse provides a model system for studying the role of replication-competent viruses in spontaneously occurring leukemias of non-T-cell lineage and neurological disease."	J Virol	1981	Aug	"Bedigian HG, Taylor BA, Meier H."	6268848					B	N	B	B	B	N	B	B	B	N	B	B	B	N
Fv-1 and H-2 genotypes of BXH RI strains	H-2 haplotype	Expression of murine leukemia viruses in the highly lymphomatous BXH-2 recombinant inbred mouse strain.	"Among 12 recombinant inbred strains of mice derived from crossing two strains, C57BL/6J and C3H/HeJ, which have a low incidence of neoplastic disease, one strain (BXH-2) has been found to have a high incidence of lymphoma, of non-T-cell origin, at an early age. The BXH-2 strain carries the Fv-1b allele and spontaneously expresses a B-tropic murine leukemia virus beginning at as early as 10 days of gestation and continuing throughout their life. No significant differences in ecotropic virus titers were observed at any age tested (16 to 17 days of gestation through 7 months), whereas xenotropic virus was first detected in lymphoid tissues of 2-month-old mice and virus titers increased with age. Dual tropic virus(es), which induced cytopathic changes on mink lung cells, was isolated from BXH-2 lymphomatous tissues. Unlike AKR mink lung focus-forming virus (N-tropic recombinant), BXH-2 dual tropic virus is B tropic and induces cytopathic changes in mouse fibroblast cultures as well. The BXH-2 mouse provides a model system for studying the role of replication-competent viruses in spontaneously occurring leukemias of non-T-cell lineage and neurological disease."	J Virol	1981	Aug	"Bedigian HG, Taylor BA, Meier H."	6268848					B	K	K	K	B	K	K	B	B	B	B	K	K	B
Distribution pattern of three chromosome 1 loci among BXH recombinant inbred strains 	Dip-1	"Mapping the gene for LTW-4, a 26,000 molecular weight major protein of mouse liver and kidney."	"The polypeptide LTW-4 has previously been shown by 2D electrophoresis to be a major soluble protein of mouse liver. We now show that it is a major soluble polypeptide of mouse kidney. The Ltw-4 locus has been mapped on Chromosome 1 using the BXD, AKXL and BXH recombinant inbred strains. The gene order is Dip-1 Rnr - (Sas-1, ald) - Ltw-4 - Mls. The map distance between (Dip-1, Rnr) and Ltw-4 is estimated to be 12.2 +/- 4.2 cM, between Sas-1 and Ltw-4 5.4 +/- 2.6, between ald and Ltw-4 7.1 +/- 4.6 cM, and between Ltw-4 and Mls 4.3 +/- 2.0 cM. The strain distribution pattern of Ltw-4 is reported for the SWXL recombinant inbred strains and for a large number of inbred strains of mice."	Mol Gen Genet	1980		"Elliott RW, Romejko C, Hohman C."	6934364	8 - 18 weeks			B = C57BL/6J; H =C3H/HeJ			B	H	B	H	H	H	H	B	B	B	H	B
Distribution pattern of three chromosome 1 loci among BXH recombinant inbred strains 	Sas-1	"Mapping the gene for LTW-4, a 26,000 molecular weight major protein of mouse liver and kidney."	"The polypeptide LTW-4 has previously been shown by 2D electrophoresis to be a major soluble protein of mouse liver. We now show that it is a major soluble polypeptide of mouse kidney. The Ltw-4 locus has been mapped on Chromosome 1 using the BXD, AKXL and BXH recombinant inbred strains. The gene order is Dip-1 Rnr - (Sas-1, ald) - Ltw-4 - Mls. The map distance between (Dip-1, Rnr) and Ltw-4 is estimated to be 12.2 +/- 4.2 cM, between Sas-1 and Ltw-4 5.4 +/- 2.6, between ald and Ltw-4 7.1 +/- 4.6 cM, and between Ltw-4 and Mls 4.3 +/- 2.0 cM. The strain distribution pattern of Ltw-4 is reported for the SWXL recombinant inbred strains and for a large number of inbred strains of mice."	Mol Gen Genet	1980		"Elliott RW, Romejko C, Hohman C."	6934364	8 - 18 weeks			B = C57BL/6J; H =C3H/HeJ			B	H	B	H	B	B	H	H	B	B	H	B
Distribution pattern of three chromosome 1 loci among BXH recombinant inbred strains 	Ltw-4	"Mapping the gene for LTW-4, a 26,000 molecular weight major protein of mouse liver and kidney."	"The polypeptide LTW-4 has previously been shown by 2D electrophoresis to be a major soluble protein of mouse liver. We now show that it is a major soluble polypeptide of mouse kidney. The Ltw-4 locus has been mapped on Chromosome 1 using the BXD, AKXL and BXH recombinant inbred strains. The gene order is Dip-1 Rnr - (Sas-1, ald) - Ltw-4 - Mls. The map distance between (Dip-1, Rnr) and Ltw-4 is estimated to be 12.2 +/- 4.2 cM, between Sas-1 and Ltw-4 5.4 +/- 2.6, between ald and Ltw-4 7.1 +/- 4.6 cM, and between Ltw-4 and Mls 4.3 +/- 2.0 cM. The strain distribution pattern of Ltw-4 is reported for the SWXL recombinant inbred strains and for a large number of inbred strains of mice."	Mol Gen Genet	1980		"Elliott RW, Romejko C, Hohman C."	6934364	8 - 18 weeks			B = C57BL/6J; H =C3H/HeJ			B	H	B	H	B	B	H	B	B	B	H	B
"inheritance of Chromosome 5 markers Pgm-1, Ric, rd, and Gus in the BXH recombinant inbred strain"	Pgm-1	Host defenses in experimental scrub typhus: mapping the gene that controls natural resistance in mice.	"Natural resistance of mice to lethal ifections of Rickettsia tsutsugamushi, strain Gilliam, is controlled by a single, autosomal, dominant gene, which we have designated Ric, with r and s representing the resistant nd susceptible alleles, respectively. Using three sets of recombinant inbred mouse strains (BXD, BXH, and BXJ), the Ric locus was mapped to Chromosome 5 closely linked to the retinal degeneration (rd) locus. This linkage was confirmed by a backcross analysis. Based on the RI strains and the C57BL/6Ty-le congenic strain (the only proven Ric-rd cross-over), we estimate the recombination frequency between Ric and rd to be 0.015. Three presumptive Ric-rd recombinants detected among 93 backcross mice may represent caes of incomplete penetrance of the resistance allele rather than recombination. Analyis of th C57BL/6JTy-le congenic strain indicates that Ric is proximal to rd on Chromosome 5. If so, the correct gene order is Pgm-1-W-Ric-rd-Gus."	J Immunol	1980	Sept	"Groves MG, Rosenstreich DL, Taylor BA, Osterman JV."	6774020	6 - 12 weeks	both		B = C57BL/6J; H =C3H/HeJ			H	H	H	B	B	H	H	B	B	B	H	H
"inheritance of Chromosome 5 markers Pgm-1, Ric, rd, and Gus in the BXH recombinant inbred strain"	Ric	Host defenses in experimental scrub typhus: mapping the gene that controls natural resistance in mice.	"Natural resistance of mice to lethal ifections of Rickettsia tsutsugamushi, strain Gilliam, is controlled by a single, autosomal, dominant gene, which we have designated Ric, with r and s representing the resistant nd susceptible alleles, respectively. Using three sets of recombinant inbred mouse strains (BXD, BXH, and BXJ), the Ric locus was mapped to Chromosome 5 closely linked to the retinal degeneration (rd) locus. This linkage was confirmed by a backcross analysis. Based on the RI strains and the C57BL/6Ty-le congenic strain (the only proven Ric-rd cross-over), we estimate the recombination frequency between Ric and rd to be 0.015. Three presumptive Ric-rd recombinants detected among 93 backcross mice may represent caes of incomplete penetrance of the resistance allele rather than recombination. Analyis of th C57BL/6JTy-le congenic strain indicates that Ric is proximal to rd on Chromosome 5. If so, the correct gene order is Pgm-1-W-Ric-rd-Gus."	J Immunol	1980	Sept	"Groves MG, Rosenstreich DL, Taylor BA, Osterman JV."	6774020	6 - 12 weeks	both		B = C57BL/6J; H =C3H/HeJ			H	H	H	B	H	H	H	B	B	B	H	H
"inheritance of Chromosome 5 markers Pgm-1, Ric, rd, and Gus in the BXH recombinant inbred strain"	rd	Host defenses in experimental scrub typhus: mapping the gene that controls natural resistance in mice.	"Natural resistance of mice to lethal ifections of Rickettsia tsutsugamushi, strain Gilliam, is controlled by a single, autosomal, dominant gene, which we have designated Ric, with r and s representing the resistant nd susceptible alleles, respectively. Using three sets of recombinant inbred mouse strains (BXD, BXH, and BXJ), the Ric locus was mapped to Chromosome 5 closely linked to the retinal degeneration (rd) locus. This linkage was confirmed by a backcross analysis. Based on the RI strains and the C57BL/6Ty-le congenic strain (the only proven Ric-rd cross-over), we estimate the recombination frequency between Ric and rd to be 0.015. Three presumptive Ric-rd recombinants detected among 93 backcross mice may represent caes of incomplete penetrance of the resistance allele rather than recombination. Analyis of th C57BL/6JTy-le congenic strain indicates that Ric is proximal to rd on Chromosome 5. If so, the correct gene order is Pgm-1-W-Ric-rd-Gus."	J Immunol	1980	Sept	"Groves MG, Rosenstreich DL, Taylor BA, Osterman JV."	6774020	6 - 12 weeks	both		B = C57BL/6J; H =C3H/HeJ			H	H	H	B	H	H	H	B	B	B	H	H
"inheritance of Chromosome 5 markers Pgm-1, Ric, rd, and Gus in the BXH recombinant inbred strain"	Gus	Host defenses in experimental scrub typhus: mapping the gene that controls natural resistance in mice.	"Natural resistance of mice to lethal ifections of Rickettsia tsutsugamushi, strain Gilliam, is controlled by a single, autosomal, dominant gene, which we have designated Ric, with r and s representing the resistant nd susceptible alleles, respectively. Using three sets of recombinant inbred mouse strains (BXD, BXH, and BXJ), the Ric locus was mapped to Chromosome 5 closely linked to the retinal degeneration (rd) locus. This linkage was confirmed by a backcross analysis. Based on the RI strains and the C57BL/6Ty-le congenic strain (the only proven Ric-rd cross-over), we estimate the recombination frequency between Ric and rd to be 0.015. Three presumptive Ric-rd recombinants detected among 93 backcross mice may represent caes of incomplete penetrance of the resistance allele rather than recombination. Analyis of th C57BL/6JTy-le congenic strain indicates that Ric is proximal to rd on Chromosome 5. If so, the correct gene order is Pgm-1-W-Ric-rd-Gus."	J Immunol	1980	Sept	"Groves MG, Rosenstreich DL, Taylor BA, Osterman JV."	6774020	6 - 12 weeks	both		B = C57BL/6J; H =C3H/HeJ			B	H	H	B	B	H	H	H	B	B	B	H
Baseline ventilatory characteristics of BXH recombinanat inbred strains	VT/TI	Genetic control of differential baseline breathing pattern.	"The purpose of the present study was to determine the genetic control of baseline breathing pattern by examining the mode of inheritance between two inbred murine strains with differential breathing characteristics. Specifically, the rapid, shallow phenotype of the C57BL/6J (B6) strain is consistently distinct from the slow, deep phenotype of the C3H/HeJ (C3) strain. The response distributions of segregant and nonsegregant progeny were compared with the two progenitor strains to determine the mode of inheritance for each ventilatory characteristic. The BXH recombinant inbred (RI) strains derived from the B6 and C3 progenitors were examined to establish strain distribution patterns for each ventilatory trait. To establish the mode of inheritance, baseline breathing frequency (f), tidal volume, and inspiratory time (TI) were measured five times in each of 178 mature male animals from the two progenitor strains and their progeny by using whole body plethysmography. With respect to f and TI, the two progenitor strains were consistently distinct, and segregation analyses of the inheritance pattern suggest that the most parsimonious genetic model for response distributions of f and TI is a two-loci model. In similar experiments conducted on 82 mature male animals from 12 BXH RI strains, each parental phenotype was represented by one or more of the RI strains. Intermediate phenotypes emerged to confirm the likelihood that parental strain differences in f and TI were determined by more than one locus. Taken together, these studies suggest that the phenotypic difference in baseline respiratory timing between male B6 and C3 mice is best explained by a genetic model that considers at least two loci as major determinants."	J Appl Physiol	1997	Mar	"Tankersley CG, Fitzgerald RS, Levitt RC, Mitzner WA, Ewart SL, Kleeberger SR."	9074977	68 - 96 days	male	10-Apr	%			63	59	59	52	58	52	70	70	50	54	53	54