Phenotype	Phenotype Details	Title	Abstract	Journal	Year	Month	Author(s)	PMID	Age	Sex	N Range	Units	A/J	A.BY/SnJ	C57BL/6J	B10.A/SgSf	AXB1	AXB2	AXB3	AXB4	AXB5	AXB6	AXB7	AXB8	AXB9	AXB10	AXB11	AXB12	AXB13	AXB14	AXB15	AXB17	AXB18	AXB19	AXB20	AXB21	AXB22	AXB23	AXB24	AXB25	BXA1	BXA2	BXA3	BXA4	BXA6	BXA7	BXA8	BXA9	BXA10	BXA11	BXA12	BXA13	BXA14	BXA15	BXA16	BXA17	BXA18	BXA19	BXA20	BXA21	BXA22	BXA23	BXA24	BXA25	BXA26	Data Entered By:

mammary patterning	ska MG pattern	Mammary gland patterning in the AXB/BXA recombinant inbred strains of mouse.		Mechanisms of Development	2000	Mar	"Howard BA, Gusterson BA"	10704854	100 days	female		%	95		0		89	100		100	0	81	U	0	U	100	U	0	100	100	0	U	88	100	65	U		100	0	U	0	0		100	U	75	100		U	0	0	100	100		100	45		U		U	U	U	100	100	100	Nathan Copeland
mammary patterning	super-numerary nipple	Mammary gland patterning in the AXB/BXA recombinant inbred strains of mouse.		Mechanisms of Development	2000	Mar	"Howard BA, Gusterson BA"	10704854	100 days	female		%	31		0		11	30		33	0	29	U	0	U	0	U	0	0	0	0	U	4	7	0	U		0	0	U	0	0		32	U	25	0		U	0	0	18	59		50	0		U		U	U	U	29	14	50	Nathan Copeland
mammary patterning	misplaced MG	Mammary gland patterning in the AXB/BXA recombinant inbred strains of mouse.		Mechanisms of Development	2000	Mar	"Howard BA, Gusterson BA"	10704854	100 days	female		%	29		0		78	100		100	0	71	U	0	U	33	U	0	100	100	0	U	80	100	76	U		75	0	U	0	0		79	U	75	100		U	0	0	73	82		93	45		U		U	U	U	85	100	50	Nathan Copeland
mammary patterning	absent #3 MG	Mammary gland patterning in the AXB/BXA recombinant inbred strains of mouse.		Mechanisms of Development	2000	Mar	"Howard BA, Gusterson BA"	10704854	100 days	female		%	55		0		0	0		0	0	0	U	0	U	67	U	0	0	0	0	U	4	0	0	U		25	0	U	0	0		11	U	0	0		U	0	0	27	12		0	0		U		U	U	U	0	0	0	Nathan Copeland
mammary patterning	normal MG pattern	Mammary gland patterning in the AXB/BXA recombinant inbred strains of mouse.		Mechanisms of Development	2000	Mar	"Howard BA, Gusterson BA"	10704854	100 days	female		%	5		100		11	0		0	100	19	U	100	U	0	U	100	0	0	100	U	12	0	35	U		0	100	U	100	100		0	U	25	0		U	100	100	0	0		0	55		U		U	U	U	12	0	0	Nathan Copeland
splenocyte mitogenic response to 20 micrograms/ml LPS		Mapping lipopolysaccharide response loci in mice using recombinant inbred and congenic strains.	"Lipopolysaccharide (LPS) induces proliferation of splenic B-cells, and this response was found to be significantly lower in A/J than in C57BL/6J (B6) mice. Several strains and substrains mirrored the high and low responses of B6 and A/J. Assessment of 26 AXB/BXA recombinant inbred (RI) mouse strains identified 23 strains with a low (A/J-like), high (B6-like), or intermediate response. The three remaining RI strains exhibited a novel hyperresponsive phenotype significantly different from that of either founder strain. RI analysis identified four suggestive loci contributing to the LPS response, two of which were confirmed by analysis of congenic strains containing the donor genomic segment from a high- or low-responder strain on the opposite background. The combination of A/J and B6 alleles fixed to homozygosity at the four suggestive loci would occur in only 1 of 256 intercross progeny, but occurred several times among the RI strains."	Genomics	1999		Matesic LE	10585765	8 to 9 wks 	both		%	0		100		105	75		140	120	150	U	80	U	75	U	U	U	U	100	U	675	450	130	U		U	95	U	150	25		40	U	80	-35		U	105	105	90	550		40	75		U		U	U	U	110	85	85	Nathan Copeland
exploratory locomotor activity	latency to enter novel side	"Genetic analysis of behavioral, neuroendocrine, and biochemical parameters in inbred rodents: initial studies in Lewis and Fischer 344 rats and in A/J and C57BL/6J mice."	"Previous work has identified inherent behavioral, neuroendocrine, and biochemical differences among inbred rodent strains that have been related to the animals' differential responsiveness to drugs of abuse or stress. In the present study, we sought to determine (1) whether there are genetic correlations among particular phenotypic traits that differ between a pair of inbred rat strains (Lewis and Fischer 344) or a pair of inbred mouse strains (A/J and C57BL/6J); (2) which of these traits might be amenable to quantitative trait locus analysis; and (3) whether additional behavioral or biochemical differences relevant to drug- or stress-responsiveness could be identified in these strains. Specifically, we measured several behavioral, neuroendocrine, and biochemical traits in parental Lewis and Fischer 344 rats and in 298 members of an F2 intercross population, as well as in parental A/J and C57BL/6J mice and in 11 of the AXB/BXA recombinant inbred mouse strains. Traits measured included exploratory locomotor activity in a novel environment; amphetamine-induced locomotor activity; several specific protein levels in striatal regions, including inhibitory G protein subunits, the dopamine transporter, the Fos family member transcription factor DeltaFosB, and the protein phosphatase inhibitor DARPP-32; and late-afternoon plasma corticosterone concentrations. Each of the traits measured in F2 rats or recombinant inbred mice appears to be influenced by multiple genes, as well as by environmental factors. There were statistically significant, albeit relatively weak, correlations among several traits in an F2 intercross population bred from Lewis and Fischer rats. Among the traits studied in Lewis and Fischer rats, one seemed most amenable to quantitative trait locus analysis: the level of the inhibitory G-protein subunit, Galphai, in the nucleus accumbens. We also found a robust genetic correlation between levels of DeltaFosB and levels of the dopamine transporter in striatal regions in AXB/BXA recombinant inbred mouse strains. While these studies demonstrate the likely complexity of the genetic factors that influence the numerous phenotypes associated with altered responsiveness to drugs of abuse and stress, they represent an initial and necessary step toward identifying specific genetic factors involved."	Brain Research	1998		Brodkin ES	9733917	35 to 42 days	male		seconds	32		10		12	13		18	23	17	U	U	U	20	U	U	U	U	U	U	U	U	U	U		U	U	U	U	U		32	U	13	U		U	U	12	U	15		U	U		U		16	U	U	U	U	U	
DAT immunoreactivity in Nac		"Genetic analysis of behavioral, neuroendocrine, and biochemical parameters in inbred rodents: initial studies in Lewis and Fischer 344 rats and in A/J and C57BL/6J mice."	"Previous work has identified inherent behavioral, neuroendocrine, and biochemical differences among inbred rodent strains that have been related to the animals' differential responsiveness to drugs of abuse or stress. In the present study, we sought to determine (1) whether there are genetic correlations among particular phenotypic traits that differ between a pair of inbred rat strains (Lewis and Fischer 344) or a pair of inbred mouse strains (A/J and C57BL/6J); (2) which of these traits might be amenable to quantitative trait locus analysis; and (3) whether additional behavioral or biochemical differences relevant to drug- or stress-responsiveness could be identified in these strains. Specifically, we measured several behavioral, neuroendocrine, and biochemical traits in parental Lewis and Fischer 344 rats and in 298 members of an F2 intercross population, as well as in parental A/J and C57BL/6J mice and in 11 of the AXB/BXA recombinant inbred mouse strains. Traits measured included exploratory locomotor activity in a novel environment; amphetamine-induced locomotor activity; several specific protein levels in striatal regions, including inhibitory G protein subunits, the dopamine transporter, the Fos family member transcription factor DeltaFosB, and the protein phosphatase inhibitor DARPP-32; and late-afternoon plasma corticosterone concentrations. Each of the traits measured in F2 rats or recombinant inbred mice appears to be influenced by multiple genes, as well as by environmental factors. There were statistically significant, albeit relatively weak, correlations among several traits in an F2 intercross population bred from Lewis and Fischer rats. Among the traits studied in Lewis and Fischer rats, one seemed most amenable to quantitative trait locus analysis: the level of the inhibitory G-protein subunit, Galphai, in the nucleus accumbens. We also found a robust genetic correlation between levels of DeltaFosB and levels of the dopamine transporter in striatal regions in AXB/BXA recombinant inbred mouse strains. While these studies demonstrate the likely complexity of the genetic factors that influence the numerous phenotypes associated with altered responsiveness to drugs of abuse and stress, they represent an initial and necessary step toward identifying specific genetic factors involved."	Brain Research	1998		Brodkin ES	9733917	35 to 42 days	male			50		90		175	180		65	160	50	U	U	U	55	U	U	U	U	U	U	U	U	U	U		U	U	U	U	U		70	U	100	U		U	U	105	U	10		U	U		U		5	U	U	U	U	U	
delta FosB immunoreactivity in dorsal striatum		"Genetic analysis of behavioral, neuroendocrine, and biochemical parameters in inbred rodents: initial studies in Lewis and Fischer 344 rats and in A/J and C57BL/6J mice."	"Previous work has identified inherent behavioral, neuroendocrine, and biochemical differences among inbred rodent strains that have been related to the animals' differential responsiveness to drugs of abuse or stress. In the present study, we sought to determine (1) whether there are genetic correlations among particular phenotypic traits that differ between a pair of inbred rat strains (Lewis and Fischer 344) or a pair of inbred mouse strains (A/J and C57BL/6J); (2) which of these traits might be amenable to quantitative trait locus analysis; and (3) whether additional behavioral or biochemical differences relevant to drug- or stress-responsiveness could be identified in these strains. Specifically, we measured several behavioral, neuroendocrine, and biochemical traits in parental Lewis and Fischer 344 rats and in 298 members of an F2 intercross population, as well as in parental A/J and C57BL/6J mice and in 11 of the AXB/BXA recombinant inbred mouse strains. Traits measured included exploratory locomotor activity in a novel environment; amphetamine-induced locomotor activity; several specific protein levels in striatal regions, including inhibitory G protein subunits, the dopamine transporter, the Fos family member transcription factor DeltaFosB, and the protein phosphatase inhibitor DARPP-32; and late-afternoon plasma corticosterone concentrations. Each of the traits measured in F2 rats or recombinant inbred mice appears to be influenced by multiple genes, as well as by environmental factors. There were statistically significant, albeit relatively weak, correlations among several traits in an F2 intercross population bred from Lewis and Fischer rats. Among the traits studied in Lewis and Fischer rats, one seemed most amenable to quantitative trait locus analysis: the level of the inhibitory G-protein subunit, Galphai, in the nucleus accumbens. We also found a robust genetic correlation between levels of DeltaFosB and levels of the dopamine transporter in striatal regions in AXB/BXA recombinant inbred mouse strains. While these studies demonstrate the likely complexity of the genetic factors that influence the numerous phenotypes associated with altered responsiveness to drugs of abuse and stress, they represent an initial and necessary step toward identifying specific genetic factors involved."	Brain Research	1998		Brodkin ES	9733917	35 to 42 days	male			35		100		150	135		70	170	60	U	U	U	175	U	U	U	U	U	U	U	U	U	U		U	U	U	U	U		100	U	150	U		U	U	100	U	115		U	U		U		35	U	U	U	U	U	
DDARPP-32 immunoreactivity in dorsal striatum		"Genetic analysis of behavioral, neuroendocrine, and biochemical parameters in inbred rodents: initial studies in Lewis and Fischer 344 rats and in A/J and C57BL/6J mice."	"Previous work has identified inherent behavioral, neuroendocrine, and biochemical differences among inbred rodent strains that have been related to the animals' differential responsiveness to drugs of abuse or stress. In the present study, we sought to determine (1) whether there are genetic correlations among particular phenotypic traits that differ between a pair of inbred rat strains (Lewis and Fischer 344) or a pair of inbred mouse strains (A/J and C57BL/6J); (2) which of these traits might be amenable to quantitative trait locus analysis; and (3) whether additional behavioral or biochemical differences relevant to drug- or stress-responsiveness could be identified in these strains. Specifically, we measured several behavioral, neuroendocrine, and biochemical traits in parental Lewis and Fischer 344 rats and in 298 members of an F2 intercross population, as well as in parental A/J and C57BL/6J mice and in 11 of the AXB/BXA recombinant inbred mouse strains. Traits measured included exploratory locomotor activity in a novel environment; amphetamine-induced locomotor activity; several specific protein levels in striatal regions, including inhibitory G protein subunits, the dopamine transporter, the Fos family member transcription factor DeltaFosB, and the protein phosphatase inhibitor DARPP-32; and late-afternoon plasma corticosterone concentrations. Each of the traits measured in F2 rats or recombinant inbred mice appears to be influenced by multiple genes, as well as by environmental factors. There were statistically significant, albeit relatively weak, correlations among several traits in an F2 intercross population bred from Lewis and Fischer rats. Among the traits studied in Lewis and Fischer rats, one seemed most amenable to quantitative trait locus analysis: the level of the inhibitory G-protein subunit, Galphai, in the nucleus accumbens. We also found a robust genetic correlation between levels of DeltaFosB and levels of the dopamine transporter in striatal regions in AXB/BXA recombinant inbred mouse strains. While these studies demonstrate the likely complexity of the genetic factors that influence the numerous phenotypes associated with altered responsiveness to drugs of abuse and stress, they represent an initial and necessary step toward identifying specific genetic factors involved."	Brain Research	1998		Brodkin ES	9733917	35 to 42 days	male			50		50		40	45		40	40	40	U	U	U	48	U	U	U	U	U	U	U	U	U	U		U	U	U	U	U		50	U	60	U		U	U	58	U	58		U	U		U		68	U	U	U	U	U	
Ucp1 mRNA levels in the retroperitoneal fat pad		Emergence of brown adipocytes in white fat in mice is under genetic control. Effects on body weight and adiposity.	"The mRNA levels for the mitochondrial uncoupling protein (UCP1) in fat tissues of A/J and C57BL/6J inbred strains of mice varied in a regional-specific manner after stimulation of adrenergic signaling by cold exposure or treatment with a beta3-adrenergic agonist. While the differences between strains were minimal in interscapular brown fat, large differences occurred in white fat tissues, particularly in retroperitoneal fat. Among the AXB recombinant inbred strains, the Ucp1 mRNA levels varied up to 130-fold. This large induction at the mRNA level was accompanied by a corresponding increase in brown adipocytes as revealed by immunohistology with anti-UCP1 antibodies. A high capacity to induce brown fat in areas of traditional white fat had no impact on the ability to gain weight in response to high fat and sucrose diets, but did correlate with the loss of weight in response to treatment with a beta3-adrenergic agonist (CL 316,243). This genetic variation in mice provides an experimental approach to identify genes controlling the induction of brown adipocytes in white fat tissues.PMID: 9664083 [PubMed - indexed for MEDLINE]------------------------------------------------------------------------DisplaySaveTextÊÊÊOrderAdd to ClipboardÊ Ê ÊÊ Ê ÊÊWrite to the Help Desk NCBI | NLM | NIH Department of Health & Human Services Freedom of Information Act | Disclaimer"	J Clin Invest	1998		"Guerra C, Koza RA"	9664083	8 wks	male		arbitrary units	700		25		50	U		U	175	U	U	1700	U	25	U	160	U	U	1500	U	U	1200	U	U		U	U	U	U	U		U	U	U	U		U	U	300	U	U		U	U		U		U	U	U	U	600	U	
emergence of brown adipocytes in white fat	retroperitoneal fat	Emergence of brown adipocytes in white fat in mice is under genetic control. Effects on body weight and adiposity.	"The mRNA levels for the mitochondrial uncoupling protein (UCP1) in fat tissues of A/J and C57BL/6J inbred strains of mice varied in a regional-specific manner after stimulation of adrenergic signaling by cold exposure or treatment with a beta3-adrenergic agonist. While the differences between strains were minimal in interscapular brown fat, large differences occurred in white fat tissues, particularly in retroperitoneal fat. Among the AXB recombinant inbred strains, the Ucp1 mRNA levels varied up to 130-fold. This large induction at the mRNA level was accompanied by a corresponding increase in brown adipocytes as revealed by immunohistology with anti-UCP1 antibodies. A high capacity to induce brown fat in areas of traditional white fat had no impact on the ability to gain weight in response to high fat and sucrose diets, but did correlate with the loss of weight in response to treatment with a beta3-adrenergic agonist (CL 316,243). This genetic variation in mice provides an experimental approach to identify genes controlling the induction of brown adipocytes in white fat tissues.PMID: 9664083 [PubMed - indexed for MEDLINE]------------------------------------------------------------------------DisplaySaveTextÊÊÊOrderAdd to ClipboardÊ Ê ÊÊ Ê ÊÊWrite to the Help Desk NCBI | NLM | NIH Department of Health & Human Services Freedom of Information Act | Disclaimer"	J Clin Invest	1998		"Guerra C, Koza RA"	9664083	8 wks	male		% total area	U		U		0.25	U		U	U	U	U	13.57	U	0.21	U	U	U	U	2.95	U	U	U	U	U		U	U	U	U	U		U	U	U	U		U	U	U	U	U		U	U		U		U	U	U	U	U	U	
Ucp1 mRNA induction 	retroperitoneal fat	Emergence of brown adipocytes in white fat in mice is under genetic control. Effects on body weight and adiposity.	"The mRNA levels for the mitochondrial uncoupling protein (UCP1) in fat tissues of A/J and C57BL/6J inbred strains of mice varied in a regional-specific manner after stimulation of adrenergic signaling by cold exposure or treatment with a beta3-adrenergic agonist. While the differences between strains were minimal in interscapular brown fat, large differences occurred in white fat tissues, particularly in retroperitoneal fat. Among the AXB recombinant inbred strains, the Ucp1 mRNA levels varied up to 130-fold. This large induction at the mRNA level was accompanied by a corresponding increase in brown adipocytes as revealed by immunohistology with anti-UCP1 antibodies. A high capacity to induce brown fat in areas of traditional white fat had no impact on the ability to gain weight in response to high fat and sucrose diets, but did correlate with the loss of weight in response to treatment with a beta3-adrenergic agonist (CL 316,243). This genetic variation in mice provides an experimental approach to identify genes controlling the induction of brown adipocytes in white fat tissues.PMID: 9664083 [PubMed - indexed for MEDLINE]------------------------------------------------------------------------DisplaySaveTextÊÊÊOrderAdd to ClipboardÊ Ê ÊÊ Ê ÊÊWrite to the Help Desk NCBI | NLM | NIH Department of Health & Human Services Freedom of Information Act | Disclaimer"	J Clin Invest	1998		"Guerra C, Koza RA"	9664083	8 wks	male		density units	U		U		40	U		U	U	U	U	1719	U	13	U	U	U	U	1490	U	U	U	U	U		U	U	U	U	U		U	U	U	U		U	U	U	U	U		U	U		U		U	U	U	U	U	U	
emergence of brown adipocytes in white fat	inguinal fat	Emergence of brown adipocytes in white fat in mice is under genetic control. Effects on body weight and adiposity.	"The mRNA levels for the mitochondrial uncoupling protein (UCP1) in fat tissues of A/J and C57BL/6J inbred strains of mice varied in a regional-specific manner after stimulation of adrenergic signaling by cold exposure or treatment with a beta3-adrenergic agonist. While the differences between strains were minimal in interscapular brown fat, large differences occurred in white fat tissues, particularly in retroperitoneal fat. Among the AXB recombinant inbred strains, the Ucp1 mRNA levels varied up to 130-fold. This large induction at the mRNA level was accompanied by a corresponding increase in brown adipocytes as revealed by immunohistology with anti-UCP1 antibodies. A high capacity to induce brown fat in areas of traditional white fat had no impact on the ability to gain weight in response to high fat and sucrose diets, but did correlate with the loss of weight in response to treatment with a beta3-adrenergic agonist (CL 316,243). This genetic variation in mice provides an experimental approach to identify genes controlling the induction of brown adipocytes in white fat tissues.PMID: 9664083 [PubMed - indexed for MEDLINE]------------------------------------------------------------------------DisplaySaveTextÊÊÊOrderAdd to ClipboardÊ Ê ÊÊ Ê ÊÊWrite to the Help Desk NCBI | NLM | NIH Department of Health & Human Services Freedom of Information Act | Disclaimer"	J Clin Invest	1998		"Guerra C, Koza RA"	9664083	8 wks	male		% total area	U		U		17.52	U		U	U	U	U	45.36	U	4.23	U	U	U	U	18.15	U	U	U	U	U		U	U	U	U	U		U	U	U	U		U	U	U	U	U		U	U		U		U	U	U	U	U	U	
Ucp1 mRNA induction 	inguinal fat	Emergence of brown adipocytes in white fat in mice is under genetic control. Effects on body weight and adiposity.	"The mRNA levels for the mitochondrial uncoupling protein (UCP1) in fat tissues of A/J and C57BL/6J inbred strains of mice varied in a regional-specific manner after stimulation of adrenergic signaling by cold exposure or treatment with a beta3-adrenergic agonist. While the differences between strains were minimal in interscapular brown fat, large differences occurred in white fat tissues, particularly in retroperitoneal fat. Among the AXB recombinant inbred strains, the Ucp1 mRNA levels varied up to 130-fold. This large induction at the mRNA level was accompanied by a corresponding increase in brown adipocytes as revealed by immunohistology with anti-UCP1 antibodies. A high capacity to induce brown fat in areas of traditional white fat had no impact on the ability to gain weight in response to high fat and sucrose diets, but did correlate with the loss of weight in response to treatment with a beta3-adrenergic agonist (CL 316,243). This genetic variation in mice provides an experimental approach to identify genes controlling the induction of brown adipocytes in white fat tissues.PMID: 9664083 [PubMed - indexed for MEDLINE]------------------------------------------------------------------------DisplaySaveTextÊÊÊOrderAdd to ClipboardÊ Ê ÊÊ Ê ÊÊWrite to the Help Desk NCBI | NLM | NIH Department of Health & Human Services Freedom of Information Act | Disclaimer"	J Clin Invest	1998		"Guerra C, Koza RA"	9664083	8 wks	male		density units	U		U		520	U		U	U	U	U	808	U	none detected	U	U	U	U	534	U	U	U	U	U		U	U	U	U	U		U	U	U	U		U	U	U	U	U		U	U		U		U	U	U	U	U	U
"effect of the beta3-adrenergic Agonist CL 316, 243 on levels of Ucp1 mRNA"	retroperitoneal white adipose tissue	Emergence of brown adipocytes in white fat in mice is under genetic control. Effects on body weight and adiposity.	"The mRNA levels for the mitochondrial uncoupling protein (UCP1) in fat tissues of A/J and C57BL/6J inbred strains of mice varied in a regional-specific manner after stimulation of adrenergic signaling by cold exposure or treatment with a beta3-adrenergic agonist. While the differences between strains were minimal in interscapular brown fat, large differences occurred in white fat tissues, particularly in retroperitoneal fat. Among the AXB recombinant inbred strains, the Ucp1 mRNA levels varied up to 130-fold. This large induction at the mRNA level was accompanied by a corresponding increase in brown adipocytes as revealed by immunohistology with anti-UCP1 antibodies. A high capacity to induce brown fat in areas of traditional white fat had no impact on the ability to gain weight in response to high fat and sucrose diets, but did correlate with the loss of weight in response to treatment with a beta3-adrenergic agonist (CL 316,243). This genetic variation in mice provides an experimental approach to identify genes controlling the induction of brown adipocytes in white fat tissues.PMID: 9664083 [PubMed - indexed for MEDLINE]------------------------------------------------------------------------DisplaySaveTextÊÊÊOrderAdd to ClipboardÊ Ê ÊÊ Ê ÊÊWrite to the Help Desk NCBI | NLM | NIH Department of Health & Human Services Freedom of Information Act | Disclaimer"	J Clin Invest	1998		"Guerra C, Koza RA"	9664083	8 wks	male		arbitrary units	237		14		9	U		U	U	U	U	1123	U	26	U	U	U	U	519	U	U	U	U	U		U	U	U	U	U		U	U	U	U		U	U	121	U	U		U	U		U		U	U	U	U	354	U
"effect of the beta3-adrenergic Agonist CL 316, 243 on levels of Ucp1 mRNA"	inguinal white adipose tissue	Emergence of brown adipocytes in white fat in mice is under genetic control. Effects on body weight and adiposity.	"The mRNA levels for the mitochondrial uncoupling protein (UCP1) in fat tissues of A/J and C57BL/6J inbred strains of mice varied in a regional-specific manner after stimulation of adrenergic signaling by cold exposure or treatment with a beta3-adrenergic agonist. While the differences between strains were minimal in interscapular brown fat, large differences occurred in white fat tissues, particularly in retroperitoneal fat. Among the AXB recombinant inbred strains, the Ucp1 mRNA levels varied up to 130-fold. This large induction at the mRNA level was accompanied by a corresponding increase in brown adipocytes as revealed by immunohistology with anti-UCP1 antibodies. A high capacity to induce brown fat in areas of traditional white fat had no impact on the ability to gain weight in response to high fat and sucrose diets, but did correlate with the loss of weight in response to treatment with a beta3-adrenergic agonist (CL 316,243). This genetic variation in mice provides an experimental approach to identify genes controlling the induction of brown adipocytes in white fat tissues.PMID: 9664083 [PubMed - indexed for MEDLINE]------------------------------------------------------------------------DisplaySaveTextÊÊÊOrderAdd to ClipboardÊ Ê ÊÊ Ê ÊÊWrite to the Help Desk NCBI | NLM | NIH Department of Health & Human Services Freedom of Information Act | Disclaimer"	J Clin Invest	1998		"Guerra C, Koza RA"	9664083	8 wks	male		arbitrary units	116		1		4.5	U		U	U	U	U	114	U	6.7	U	U	U	U	222	U	U	U	U	U		U	U	U	U	U		U	U	U	U		U	U	88	U	U		U	U		U		U	U	U	U	233	U
"effect of the beta3-adrenergic Agonist CL 316, 243 on levels of body weight"	pretreatment	Emergence of brown adipocytes in white fat in mice is under genetic control. Effects on body weight and adiposity.	"The mRNA levels for the mitochondrial uncoupling protein (UCP1) in fat tissues of A/J and C57BL/6J inbred strains of mice varied in a regional-specific manner after stimulation of adrenergic signaling by cold exposure or treatment with a beta3-adrenergic agonist. While the differences between strains were minimal in interscapular brown fat, large differences occurred in white fat tissues, particularly in retroperitoneal fat. Among the AXB recombinant inbred strains, the Ucp1 mRNA levels varied up to 130-fold. This large induction at the mRNA level was accompanied by a corresponding increase in brown adipocytes as revealed by immunohistology with anti-UCP1 antibodies. A high capacity to induce brown fat in areas of traditional white fat had no impact on the ability to gain weight in response to high fat and sucrose diets, but did correlate with the loss of weight in response to treatment with a beta3-adrenergic agonist (CL 316,243). This genetic variation in mice provides an experimental approach to identify genes controlling the induction of brown adipocytes in white fat tissues.PMID: 9664083 [PubMed - indexed for MEDLINE]------------------------------------------------------------------------DisplaySaveTextÊÊÊOrderAdd to ClipboardÊ Ê ÊÊ Ê ÊÊWrite to the Help Desk NCBI | NLM | NIH Department of Health & Human Services Freedom of Information Act | Disclaimer"	J Clin Invest	1998		"Guerra C, Koza RA"	9664083	8 wks	male		g	34.2		49.6		42.5	U		U	U	U	U	41.3	U	43.6	U	U	U	U	46.3	U	U	U	U	U		U	U	U	U	U		U	U	U	U		U	U	32.4	U	U		U	U		U		U	U	U	U	41.5	U
"effect of the beta3-adrenergic Agonist CL 316, 243 on levels of body weight"	post treatment	Emergence of brown adipocytes in white fat in mice is under genetic control. Effects on body weight and adiposity.	"The mRNA levels for the mitochondrial uncoupling protein (UCP1) in fat tissues of A/J and C57BL/6J inbred strains of mice varied in a regional-specific manner after stimulation of adrenergic signaling by cold exposure or treatment with a beta3-adrenergic agonist. While the differences between strains were minimal in interscapular brown fat, large differences occurred in white fat tissues, particularly in retroperitoneal fat. Among the AXB recombinant inbred strains, the Ucp1 mRNA levels varied up to 130-fold. This large induction at the mRNA level was accompanied by a corresponding increase in brown adipocytes as revealed by immunohistology with anti-UCP1 antibodies. A high capacity to induce brown fat in areas of traditional white fat had no impact on the ability to gain weight in response to high fat and sucrose diets, but did correlate with the loss of weight in response to treatment with a beta3-adrenergic agonist (CL 316,243). This genetic variation in mice provides an experimental approach to identify genes controlling the induction of brown adipocytes in white fat tissues.PMID: 9664083 [PubMed - indexed for MEDLINE]------------------------------------------------------------------------DisplaySaveTextÊÊÊOrderAdd to ClipboardÊ Ê ÊÊ Ê ÊÊWrite to the Help Desk NCBI | NLM | NIH Department of Health & Human Services Freedom of Information Act | Disclaimer"	J Clin Invest	1998		"Guerra C, Koza RA"	9664083	8 wks	male		g	31		44.3		41.3	U		U	U	U	U	32.1	U	37.7	U	U	U	U	37.5	U	U	U	U	U		U	U	U	U	U		U	U	U	U		U	U	29.6	U	U		U	U		U		U	U	U	U	34.9	U
"effect of the beta3-adrenergic Agonist CL 316, 243 on levels of food intake"	(-)agonist	Emergence of brown adipocytes in white fat in mice is under genetic control. Effects on body weight and adiposity.	"The mRNA levels for the mitochondrial uncoupling protein (UCP1) in fat tissues of A/J and C57BL/6J inbred strains of mice varied in a regional-specific manner after stimulation of adrenergic signaling by cold exposure or treatment with a beta3-adrenergic agonist. While the differences between strains were minimal in interscapular brown fat, large differences occurred in white fat tissues, particularly in retroperitoneal fat. Among the AXB recombinant inbred strains, the Ucp1 mRNA levels varied up to 130-fold. This large induction at the mRNA level was accompanied by a corresponding increase in brown adipocytes as revealed by immunohistology with anti-UCP1 antibodies. A high capacity to induce brown fat in areas of traditional white fat had no impact on the ability to gain weight in response to high fat and sucrose diets, but did correlate with the loss of weight in response to treatment with a beta3-adrenergic agonist (CL 316,243). This genetic variation in mice provides an experimental approach to identify genes controlling the induction of brown adipocytes in white fat tissues.PMID: 9664083 [PubMed - indexed for MEDLINE]------------------------------------------------------------------------DisplaySaveTextÊÊÊOrderAdd to ClipboardÊ Ê ÊÊ Ê ÊÊWrite to the Help Desk NCBI | NLM | NIH Department of Health & Human Services Freedom of Information Act | Disclaimer"	J Clin Invest	1998		"Guerra C, Koza RA"	9664083	8 wks	male		g/wk/mouse	15.5		18.2		19.4	U		U	U	U	U	16.4	U	15.5	U	U	U	U	19	U	U	U	U	U		U	U	U	U	U		U	U	U	U		U	U	13.9	U	U		U	U		U		U	U	U	U	14	U
"effect of the beta3-adrenergic Agonist CL 316, 243 on levels of food intake"	(+)agonist	Emergence of brown adipocytes in white fat in mice is under genetic control. Effects on body weight and adiposity.	"The mRNA levels for the mitochondrial uncoupling protein (UCP1) in fat tissues of A/J and C57BL/6J inbred strains of mice varied in a regional-specific manner after stimulation of adrenergic signaling by cold exposure or treatment with a beta3-adrenergic agonist. While the differences between strains were minimal in interscapular brown fat, large differences occurred in white fat tissues, particularly in retroperitoneal fat. Among the AXB recombinant inbred strains, the Ucp1 mRNA levels varied up to 130-fold. This large induction at the mRNA level was accompanied by a corresponding increase in brown adipocytes as revealed by immunohistology with anti-UCP1 antibodies. A high capacity to induce brown fat in areas of traditional white fat had no impact on the ability to gain weight in response to high fat and sucrose diets, but did correlate with the loss of weight in response to treatment with a beta3-adrenergic agonist (CL 316,243). This genetic variation in mice provides an experimental approach to identify genes controlling the induction of brown adipocytes in white fat tissues."	J Clin Invest	1998		"Guerra C, Koza RA"	9664083	8 wks	male		g/wk/mouse	17.6		13.2		15.3	U		U	U	U	U	14	U	11.6	U	U	U	U	15.5	U	U	U	U	U		U	U	U	U	U		U	U	U	U		U	U	11.7	U	U		U	U		U		U	U	U	U	15.2	U
"effect of the beta3-adrenergic Agonist CL 316, 243 on levels of fat pad weights"	interscapular brown adipose tissue	Emergence of brown adipocytes in white fat in mice is under genetic control. Effects on body weight and adiposity.	"The mRNA levels for the mitochondrial uncoupling protein (UCP1) in fat tissues of A/J and C57BL/6J inbred strains of mice varied in a regional-specific manner after stimulation of adrenergic signaling by cold exposure or treatment with a beta3-adrenergic agonist. While the differences between strains were minimal in interscapular brown fat, large differences occurred in white fat tissues, particularly in retroperitoneal fat. Among the AXB recombinant inbred strains, the Ucp1 mRNA levels varied up to 130-fold. This large induction at the mRNA level was accompanied by a corresponding increase in brown adipocytes as revealed by immunohistology with anti-UCP1 antibodies. A high capacity to induce brown fat in areas of traditional white fat had no impact on the ability to gain weight in response to high fat and sucrose diets, but did correlate with the loss of weight in response to treatment with a beta3-adrenergic agonist (CL 316,243). This genetic variation in mice provides an experimental approach to identify genes controlling the induction of brown adipocytes in white fat tissues."	J Clin Invest	1998		"Guerra C, Koza RA"	9664083	8 wks	male		g	0.11		0.23		0.2	U		U	U	U	U	0.1	U	0.13	U	U	U	U	0.15	U	U	U	U	U		U	U	U	U	U		U	U	U	U		U	U	0.11	U	U		U	U		U		U	U	U	U	0.16	U
"effect of the beta3-adrenergic Agonist CL 316, 243 on levels of fat pad weights"	epididymal white adipose tissue	Emergence of brown adipocytes in white fat in mice is under genetic control. Effects on body weight and adiposity.	"The mRNA levels for the mitochondrial uncoupling protein (UCP1) in fat tissues of A/J and C57BL/6J inbred strains of mice varied in a regional-specific manner after stimulation of adrenergic signaling by cold exposure or treatment with a beta3-adrenergic agonist. While the differences between strains were minimal in interscapular brown fat, large differences occurred in white fat tissues, particularly in retroperitoneal fat. Among the AXB recombinant inbred strains, the Ucp1 mRNA levels varied up to 130-fold. This large induction at the mRNA level was accompanied by a corresponding increase in brown adipocytes as revealed by immunohistology with anti-UCP1 antibodies. A high capacity to induce brown fat in areas of traditional white fat had no impact on the ability to gain weight in response to high fat and sucrose diets, but did correlate with the loss of weight in response to treatment with a beta3-adrenergic agonist (CL 316,243). This genetic variation in mice provides an experimental approach to identify genes controlling the induction of brown adipocytes in white fat tissues."	J Clin Invest	1998		"Guerra C, Koza RA"	9664083	8 wks	male		g	0.91		1.55		0.83	U		U	U	U	U	0.55	U	1.67	U	U	U	U	1.27	U	U	U	U	U		U	U	U	U	U		U	U	U	U		U	U	0.37	U	U		U	U		U		U	U	U	U	1.52	U
"effect of the beta3-adrenergic Agonist CL 316, 243 on levels of fat pad weights"	inguinal white adipose tissue	Emergence of brown adipocytes in white fat in mice is under genetic control. Effects on body weight and adiposity.	"The mRNA levels for the mitochondrial uncoupling protein (UCP1) in fat tissues of A/J and C57BL/6J inbred strains of mice varied in a regional-specific manner after stimulation of adrenergic signaling by cold exposure or treatment with a beta3-adrenergic agonist. While the differences between strains were minimal in interscapular brown fat, large differences occurred in white fat tissues, particularly in retroperitoneal fat. Among the AXB recombinant inbred strains, the Ucp1 mRNA levels varied up to 130-fold. This large induction at the mRNA level was accompanied by a corresponding increase in brown adipocytes as revealed by immunohistology with anti-UCP1 antibodies. A high capacity to induce brown fat in areas of traditional white fat had no impact on the ability to gain weight in response to high fat and sucrose diets, but did correlate with the loss of weight in response to treatment with a beta3-adrenergic agonist (CL 316,243). This genetic variation in mice provides an experimental approach to identify genes controlling the induction of brown adipocytes in white fat tissues."	J Clin Invest	1998		"Guerra C, Koza RA"	9664083	8 wks	male		g	0.57		1.61		1.41	U		U	U	U	U	0.55	U	1.15	U	U	U	U	0.94	U	U	U	U	U		U	U	U	U	U		U	U	U	U		U	U	0.3	U	U		U	U		U		U	U	U	U	0.83	U
"effect of the beta3-adrenergic Agonist CL 316, 243 on levels of fat pad weights"	mesenteric white adipose tissue	Emergence of brown adipocytes in white fat in mice is under genetic control. Effects on body weight and adiposity.	"The mRNA levels for the mitochondrial uncoupling protein (UCP1) in fat tissues of A/J and C57BL/6J inbred strains of mice varied in a regional-specific manner after stimulation of adrenergic signaling by cold exposure or treatment with a beta3-adrenergic agonist. While the differences between strains were minimal in interscapular brown fat, large differences occurred in white fat tissues, particularly in retroperitoneal fat. Among the AXB recombinant inbred strains, the Ucp1 mRNA levels varied up to 130-fold. This large induction at the mRNA level was accompanied by a corresponding increase in brown adipocytes as revealed by immunohistology with anti-UCP1 antibodies. A high capacity to induce brown fat in areas of traditional white fat had no impact on the ability to gain weight in response to high fat and sucrose diets, but did correlate with the loss of weight in response to treatment with a beta3-adrenergic agonist (CL 316,243). This genetic variation in mice provides an experimental approach to identify genes controlling the induction of brown adipocytes in white fat tissues."	J Clin Invest	1998		"Guerra C, Koza RA"	9664083	8 wks	male		g	0.26		0.67		0.4	U		U	U	U	U	0.13	U	0.92	U	U	U	U	0.55	U	U	U	U	U		U	U	U	U	U		U	U	U	U		U	U	0.16	U	U		U	U		U		U	U	U	U	0.38	U
"effect of the beta3-adrenergic Agonist CL 316, 243 on levels of fat pad weights"	retroperitoneal white adipose tissue	Emergence of brown adipocytes in white fat in mice is under genetic control. Effects on body weight and adiposity.	"The mRNA levels for the mitochondrial uncoupling protein (UCP1) in fat tissues of A/J and C57BL/6J inbred strains of mice varied in a regional-specific manner after stimulation of adrenergic signaling by cold exposure or treatment with a beta3-adrenergic agonist. While the differences between strains were minimal in interscapular brown fat, large differences occurred in white fat tissues, particularly in retroperitoneal fat. Among the AXB recombinant inbred strains, the Ucp1 mRNA levels varied up to 130-fold. This large induction at the mRNA level was accompanied by a corresponding increase in brown adipocytes as revealed by immunohistology with anti-UCP1 antibodies. A high capacity to induce brown fat in areas of traditional white fat had no impact on the ability to gain weight in response to high fat and sucrose diets, but did correlate with the loss of weight in response to treatment with a beta3-adrenergic agonist (CL 316,243). This genetic variation in mice provides an experimental approach to identify genes controlling the induction of brown adipocytes in white fat tissues."	J Clin Invest	1998		"Guerra C, Koza RA"	9664083	8 wks	male		g	0.19		0.43		0.28	U		U	U	U	U	0.1	U	0.48	U	U	U	U	0.2	U	U	U	U	U		U	U	U	U	U		U	U	U	U		U	U	0.07	U	U		U	U		U		U	U	U	U	0.32	U
frequency of cleft lip with exposure to phenytoin		Genome scan for teratogen-induced clefting susceptibility loci in the mouse: evidence of both allelic and locus heterogeneity distinguishing cleft lip and cleft palate.	"Nonsyndromic clefting of the lip and palate in humans has a highly complex etiology, with both multiple genetic loci and exposure to teratogens influencing susceptibility. Previous studies using mouse models have examined only very small portions of the genome. Here we report the findings of a genome-wide search for susceptibility genes for teratogen-induced clefting in the AXB and BXA set of recombinant inbred mouse strains. We compare results obtained using phenytoin (which induces cleft lip) and 6-aminonicotinamide (which induces cleft palate). We use a new statistical approach based on logistic regression suitable for these categorical data to identify several chromosomal regions as possible locations of clefting susceptibility loci, and we review candidate genes located within each region. Because cleft lip and cleft palate do not frequently co-aggregate in human families and because these structures arise semi-independently during development, these disorders are usually considered to be distinct in etiology. Our data, however, implicate several of the same chromosomal regions for both forms of clefting when teratogen-induced. Furthermore, different parental strain alleles are usually associated with clefting of the lip versus that of the palate (i.e., allelic heterogeneity). Because several other chromosomal regions are associated with only one form of clefting, locus heterogeneity also appears to be involved. Our findings in this mouse model suggest several priority areas for evaluation in human epidemiological studies."	Proc Natl Acad Sci USA	1997		"Diehl SR, Erickson RP"	9144220	fetuses	both		% clefting	43.1		1.1		U	12		U	5.9	34.3	4	U	U	U	U	U	16.4	U	0	1.8	U	U	U	U		U	U	U	U	U		U	U	U	1.7		U	U	U	U	0		U	U		U		U	U	U	U	U	U
frequency of cleft palate with exposure to 6-AN		Genome scan for teratogen-induced clefting susceptibility loci in the mouse: evidence of both allelic and locus heterogeneity distinguishing cleft lip and cleft palate.	"Nonsyndromic clefting of the lip and palate in humans has a highly complex etiology, with both multiple genetic loci and exposure to teratogens influencing susceptibility. Previous studies using mouse models have examined only very small portions of the genome. Here we report the findings of a genome-wide search for susceptibility genes for teratogen-induced clefting in the AXB and BXA set of recombinant inbred mouse strains. We compare results obtained using phenytoin (which induces cleft lip) and 6-aminonicotinamide (which induces cleft palate). We use a new statistical approach based on logistic regression suitable for these categorical data to identify several chromosomal regions as possible locations of clefting susceptibility loci, and we review candidate genes located within each region. Because cleft lip and cleft palate do not frequently co-aggregate in human families and because these structures arise semi-independently during development, these disorders are usually considered to be distinct in etiology. Our data, however, implicate several of the same chromosomal regions for both forms of clefting when teratogen-induced. Furthermore, different parental strain alleles are usually associated with clefting of the lip versus that of the palate (i.e., allelic heterogeneity). Because several other chromosomal regions are associated with only one form of clefting, locus heterogeneity also appears to be involved. Our findings in this mouse model suggest several priority areas for evaluation in human epidemiological studies."	Proc Natl Acad Sci USA	1997		"Diehl SR, Erickson RP"	9144220	fetuses	both		% clefting	54.1		8.9		U	5.5		U	50	22	U	U	86.4	U	U	62	U	U	32.7	21.6	U	U	U	U		U	U	U	U	39		62.2	U	U	U		U	U	U	U	85.9		U	U		U		U	U	U	U	U	U
induction of anti-cardiac sacrolemmal antibody in Coxsackievirus B3-infected lines		Genetic control of Coxsackievirus B3-induced heart-specific autoantibodies associated with chronic myocarditis.	"Cardiac-specific autoantibodies to sarcolemmal and cardiac myosin antigens observed during the chronic phase of Coxsackievirus B3-induced myocarditis appear to be under autosomal recessive control. This observation is based on examination of F1 hybrids bred from A/J mice which develop chronic myocarditis and C57BL/6J mice which resolve the virus-induced lesions. Previous mouse studies demonstrated that the prevalence of heart-specific autoantibodies varied with the H-2 complex. However, in 25 H-2 congenic mouse strains the strain background was the predominant determinant of autoantibody presence. Recently, we extended our genetic evaluation of the chromosomal locations governing autoantibody responses by examining 25 AXB and BXA recombinant inbred strains. Two populations of heart-specific autoantibodies were demonstrated against sarcolemmal and cardiac myosin antigens. Analyses of the AXB/BXA strain distribution patterns for these two traits revealed that the anti-sarcolemmal response was controlled by a gene(s) linked to Np-2 and Ter alpha loci on chromosome 14. Linkage could not be assigned for the anti-cardiac myosin response."	Clin Exp Immunol	1991		"Traystman MD, Beisel KW"	1657464	100 days	both		% prevalence	36		0		9	48		U	0	64	0	9	U	0	U	U	U	U	47	17	18	0	0	0		44	U	12	U	U		U	50	U	30		0	0	6	U	U		U	U		16		U	73	63	18	17	U
production of cardiac myosin autoantibodies	cardiac myosin autoantibody titre	Genetic control of Coxsackievirus B3-induced heart-specific autoantibodies associated with chronic myocarditis.	"Cardiac-specific autoantibodies to sarcolemmal and cardiac myosin antigens observed during the chronic phase of Coxsackievirus B3-induced myocarditis appear to be under autosomal recessive control. This observation is based on examination of F1 hybrids bred from A/J mice which develop chronic myocarditis and C57BL/6J mice which resolve the virus-induced lesions. Previous mouse studies demonstrated that the prevalence of heart-specific autoantibodies varied with the H-2 complex. However, in 25 H-2 congenic mouse strains the strain background was the predominant determinant of autoantibody presence. Recently, we extended our genetic evaluation of the chromosomal locations governing autoantibody responses by examining 25 AXB and BXA recombinant inbred strains. Two populations of heart-specific autoantibodies were demonstrated against sarcolemmal and cardiac myosin antigens. Analyses of the AXB/BXA strain distribution patterns for these two traits revealed that the anti-sarcolemmal response was controlled by a gene(s) linked to Np-2 and Ter alpha loci on chromosome 14. Linkage could not be assigned for the anti-cardiac myosin response."	Clin Exp Immunol	1991		"Traystman MD, Beisel KW"	1657464	100 days	both			640		80		160	320		U	160	320	80	U	U	80	U	U	U	U	160	320	160	80	320	160		320	U	640	U	U		U	320	U	320		320	160	160	U	U		U	U		160		U	160	160	320	160	U
production of cardiac myosin autoantibodies	"residual activity after adsorption, heart"	Genetic control of Coxsackievirus B3-induced heart-specific autoantibodies associated with chronic myocarditis.	"Cardiac-specific autoantibodies to sarcolemmal and cardiac myosin antigens observed during the chronic phase of Coxsackievirus B3-induced myocarditis appear to be under autosomal recessive control. This observation is based on examination of F1 hybrids bred from A/J mice which develop chronic myocarditis and C57BL/6J mice which resolve the virus-induced lesions. Previous mouse studies demonstrated that the prevalence of heart-specific autoantibodies varied with the H-2 complex. However, in 25 H-2 congenic mouse strains the strain background was the predominant determinant of autoantibody presence. Recently, we extended our genetic evaluation of the chromosomal locations governing autoantibody responses by examining 25 AXB and BXA recombinant inbred strains. Two populations of heart-specific autoantibodies were demonstrated against sarcolemmal and cardiac myosin antigens. Analyses of the AXB/BXA strain distribution patterns for these two traits revealed that the anti-sarcolemmal response was controlled by a gene(s) linked to Np-2 and Ter alpha loci on chromosome 14. Linkage could not be assigned for the anti-cardiac myosin response."	Clin Exp Immunol	1991		"Traystman MD, Beisel KW"	1657464	100 days	both		%	27		0		0	44		U	0	21	U	U	U	U	U	U	U	U	o	26	13	U	U	0		25	U	32	U	U		U	0	U	0		0	U	0	U	U		U	U		0		U	0	27	36	36	U	
production of cardiac myosin autoantibodies	residual activity after adsorption skeletal	Genetic control of Coxsackievirus B3-induced heart-specific autoantibodies associated with chronic myocarditis.	"Cardiac-specific autoantibodies to sarcolemmal and cardiac myosin antigens observed during the chronic phase of Coxsackievirus B3-induced myocarditis appear to be under autosomal recessive control. This observation is based on examination of F1 hybrids bred from A/J mice which develop chronic myocarditis and C57BL/6J mice which resolve the virus-induced lesions. Previous mouse studies demonstrated that the prevalence of heart-specific autoantibodies varied with the H-2 complex. However, in 25 H-2 congenic mouse strains the strain background was the predominant determinant of autoantibody presence. Recently, we extended our genetic evaluation of the chromosomal locations governing autoantibody responses by examining 25 AXB and BXA recombinant inbred strains. Two populations of heart-specific autoantibodies were demonstrated against sarcolemmal and cardiac myosin antigens. Analyses of the AXB/BXA strain distribution patterns for these two traits revealed that the anti-sarcolemmal response was controlled by a gene(s) linked to Np-2 and Ter alpha loci on chromosome 14. Linkage could not be assigned for the anti-cardiac myosin response."	Clin Exp Immunol	1991		"Traystman MD, Beisel KW"	1657464	100 days	both		%	0		0		0	0		U	0	0	U	U	U	U	U	U	U	U	0	0	0	U	U	0		0	U	0	U	U		U	0	U	0		0	U	0	U	U		U	U		0		U	0	0	0	0	U	
susceptibility to Coxsackievirus B3-induced chronic  myocarditis	fibrocalcific lesions	Susceptibility to Coxsackievirus B3-induced chronic myocarditis maps near the murine Tcr alpha and Myhc alpha loci on chromosome 14.	"This study was undertaken to determine the genetic control of host susceptibility to coxsackievirus B3 (CVB3)-induced chronic myocarditis in a mouse model. An autosomal recessive autoimmune myocardial disease (amd) gene (possibly more than one gene), which determined susceptibility to CVB3-induced chronic myocarditis in the A/J and DBA/2J inbred mouse strains, was mapped to a segment of chromosome 14. Data from both the AXB/BXA recombinant inbred (RI) strains and the B10.D2(57N) H-8b congenic mice supported this linkage relationship. Analysis of the AXB/BXA RI strain distribution patterns suggested that amd maps distal to the Np-2, Tcr alpha, and Myhc alpha loci."	Am J Pathol	1991		"Traystman MD, Chow LH"	1848043	2 wks	both		% prevalence	40		14		9	71		U	48	93	44	0	U	55	U	U	U	U	84	20	4	20	0	48		100	U	50	U	U		U	30	U	0		18	50	0	U	U		U	U		32		U	55	55	23	11	U	
susceptibility to Coxsackievirus B3-induced chronic  myocarditis	"fibrocalcific lesions, pathologic index"	Susceptibility to Coxsackievirus B3-induced chronic myocarditis maps near the murine Tcr alpha and Myhc alpha loci on chromosome 14.	"This study was undertaken to determine the genetic control of host susceptibility to coxsackievirus B3 (CVB3)-induced chronic myocarditis in a mouse model. An autosomal recessive autoimmune myocardial disease (amd) gene (possibly more than one gene), which determined susceptibility to CVB3-induced chronic myocarditis in the A/J and DBA/2J inbred mouse strains, was mapped to a segment of chromosome 14. Data from both the AXB/BXA recombinant inbred (RI) strains and the B10.D2(57N) H-8b congenic mice supported this linkage relationship. Analysis of the AXB/BXA RI strain distribution patterns suggested that amd maps distal to the Np-2, Tcr alpha, and Myhc alpha loci."	Am J Pathol	1991		"Traystman MD, Chow LH"	1848043	2 wks	both			1.5		0.2		0.1	1.7		U	0.8	2.2	0.5	0	U	1	U	U	U	U	1.8	0.3	0.2	0.4	0	1		2.4	U	0.6	U	U		U	0.4	U	0		0.2	1.1	0	U	U		U	U		0.5		U	0.9	1.4	0.8	0.2	U	
susceptibility to Coxsackievirus B3-induced chronic  myocarditis	chronic myocarditis	Susceptibility to Coxsackievirus B3-induced chronic myocarditis maps near the murine Tcr alpha and Myhc alpha loci on chromosome 14.	"This study was undertaken to determine the genetic control of host susceptibility to coxsackievirus B3 (CVB3)-induced chronic myocarditis in a mouse model. An autosomal recessive autoimmune myocardial disease (amd) gene (possibly more than one gene), which determined susceptibility to CVB3-induced chronic myocarditis in the A/J and DBA/2J inbred mouse strains, was mapped to a segment of chromosome 14. Data from both the AXB/BXA recombinant inbred (RI) strains and the B10.D2(57N) H-8b congenic mice supported this linkage relationship. Analysis of the AXB/BXA RI strain distribution patterns suggested that amd maps distal to the Np-2, Tcr alpha, and Myhc alpha loci."	Am J Pathol	1991		"Traystman MD, Chow LH"	1848043	2 wks	both		% prevalence	18		1		0	48		U	0	47	0	0	U	36	U	U	U	U	16	0	0	0	0	28		40	U	0	U	U		U	30	U	0		0	13	0	U	U		U	U		0		U	0	25	15	4	U	
exploration in the light-dark paradigm	number of transitions during a 10-min session	Genetic analysis of anxiety-related behaviors and responses to benzodiazepine-related drugs in AXB and BXA recombinant inbred mouse strains.	"Recombinant inbred (RI) strains derived from the C57BL/6J and A/J mouse strains were used for behavioral studies designed to estimate the number and location of chromosomal loci responsible for anxiety-related behaviors and differential sensitivity to agonists and inverse agonists of the gamma-aminobutyric acidA (GABAA)/benzodiazepine receptor complex. The phenotypes of the parental inbred strains and of 28 RI strains were characterized for the number of transitions in the light<-->dark exploratory model, anxiolytic response to diazepam, vertical and ambulatory activities in an open field, and sensitivity to the convulsant properties of methyl-beta-carboline-3-carboxylate (beta-CCM). The strain distribution patterns and estimates of the minimal number of loci obtained for each trait suggest that multiple chromosomal loci contribute to differences in anxiety-related behavioral phenotypes and the behavioral responses to diazepam and beta-CCM between C57BL/6J and A/J mice. The best probabilities of linkage were found between the variables characterizing response to diazepam and loci on chromosomes 1 (Xmv-41) and 10 (D10Mit2) and between the sensitivity to the convulsant actions of beta-CCM and locus D15Mit5 on chromosome 15."	Behav Genet	1995		"Mathis C, Neumann PE"	8540894	5 to 7 wks	both	10 to 20		10		69		35	45		26	42	40	U	50	U	23	28	U	19	U	17	U	36	37	37	U		36	40	U	U	26		10	U	55	31		U	26	39	32	25		U	U		U		U	U	U	36	21	50	
ambulatory activity	number of transitions during a 5-min session	Genetic analysis of anxiety-related behaviors and responses to benzodiazepine-related drugs in AXB and BXA recombinant inbred mouse strains.	"Recombinant inbred (RI) strains derived from the C57BL/6J and A/J mouse strains were used for behavioral studies designed to estimate the number and location of chromosomal loci responsible for anxiety-related behaviors and differential sensitivity to agonists and inverse agonists of the gamma-aminobutyric acidA (GABAA)/benzodiazepine receptor complex. The phenotypes of the parental inbred strains and of 28 RI strains were characterized for the number of transitions in the light<-->dark exploratory model, anxiolytic response to diazepam, vertical and ambulatory activities in an open field, and sensitivity to the convulsant properties of methyl-beta-carboline-3-carboxylate (beta-CCM). The strain distribution patterns and estimates of the minimal number of loci obtained for each trait suggest that multiple chromosomal loci contribute to differences in anxiety-related behavioral phenotypes and the behavioral responses to diazepam and beta-CCM between C57BL/6J and A/J mice. The best probabilities of linkage were found between the variables characterizing response to diazepam and loci on chromosomes 1 (Xmv-41) and 10 (D10Mit2) and between the sensitivity to the convulsant actions of beta-CCM and locus D15Mit5 on chromosome 15."	Behav Genet	1995		"Mathis C, Neumann PE"	8540894	5 to 7 wks	both	10 to 20		100		950		600	680		380	500	830	U	800	U	680	350	U	420	680	440	U	600	600	420	U		540	630	U	650	450		200	U	850	400		U	360	650	380	560		U	U		U		U	U	U	820	350	680	
vertical activity	number of transitions during a 5-min session	Genetic analysis of anxiety-related behaviors and responses to benzodiazepine-related drugs in AXB and BXA recombinant inbred mouse strains.	"Recombinant inbred (RI) strains derived from the C57BL/6J and A/J mouse strains were used for behavioral studies designed to estimate the number and location of chromosomal loci responsible for anxiety-related behaviors and differential sensitivity to agonists and inverse agonists of the gamma-aminobutyric acidA (GABAA)/benzodiazepine receptor complex. The phenotypes of the parental inbred strains and of 28 RI strains were characterized for the number of transitions in the light<-->dark exploratory model, anxiolytic response to diazepam, vertical and ambulatory activities in an open field, and sensitivity to the convulsant properties of methyl-beta-carboline-3-carboxylate (beta-CCM). The strain distribution patterns and estimates of the minimal number of loci obtained for each trait suggest that multiple chromosomal loci contribute to differences in anxiety-related behavioral phenotypes and the behavioral responses to diazepam and beta-CCM between C57BL/6J and A/J mice. The best probabilities of linkage were found between the variables characterizing response to diazepam and loci on chromosomes 1 (Xmv-41) and 10 (D10Mit2) and between the sensitivity to the convulsant actions of beta-CCM and locus D15Mit5 on chromosome 15."	Behav Genet	1995		"Mathis C, Neumann PE"	8540894	5 to 7 wks	both	10 to 20		4		55		30	85		12	18	70	U	40	U	29	11	U	33	62	21	U	38	56	45	U		29	29	U	42	29		20	U	72	34		U	10	17	24	43		U	U		U		U	U	U	44	19	55	
exploration under vehicle	number of transitions during a 10-min session	Genetic analysis of anxiety-related behaviors and responses to benzodiazepine-related drugs in AXB and BXA recombinant inbred mouse strains.	"Recombinant inbred (RI) strains derived from the C57BL/6J and A/J mouse strains were used for behavioral studies designed to estimate the number and location of chromosomal loci responsible for anxiety-related behaviors and differential sensitivity to agonists and inverse agonists of the gamma-aminobutyric acidA (GABAA)/benzodiazepine receptor complex. The phenotypes of the parental inbred strains and of 28 RI strains were characterized for the number of transitions in the light<-->dark exploratory model, anxiolytic response to diazepam, vertical and ambulatory activities in an open field, and sensitivity to the convulsant properties of methyl-beta-carboline-3-carboxylate (beta-CCM). The strain distribution patterns and estimates of the minimal number of loci obtained for each trait suggest that multiple chromosomal loci contribute to differences in anxiety-related behavioral phenotypes and the behavioral responses to diazepam and beta-CCM between C57BL/6J and A/J mice. The best probabilities of linkage were found between the variables characterizing response to diazepam and loci on chromosomes 1 (Xmv-41) and 10 (D10Mit2) and between the sensitivity to the convulsant actions of beta-CCM and locus D15Mit5 on chromosome 15."	Behav Genet	1995		"Mathis C, Neumann PE"	8540894	5 to 7 wks	both	9 to 20		10		40		28	40		17	20	28	U	30	U	30	17	U	17	28	12	U	30	20	20	U		26	30	U	30	20		10	U	30	30		U	20	38	20	30		U	U		U		U	U	U	26	13	38	
exploration under diazepam	number of transitions during a 10-min session	Genetic analysis of anxiety-related behaviors and responses to benzodiazepine-related drugs in AXB and BXA recombinant inbred mouse strains.	"Recombinant inbred (RI) strains derived from the C57BL/6J and A/J mouse strains were used for behavioral studies designed to estimate the number and location of chromosomal loci responsible for anxiety-related behaviors and differential sensitivity to agonists and inverse agonists of the gamma-aminobutyric acidA (GABAA)/benzodiazepine receptor complex. The phenotypes of the parental inbred strains and of 28 RI strains were characterized for the number of transitions in the light<-->dark exploratory model, anxiolytic response to diazepam, vertical and ambulatory activities in an open field, and sensitivity to the convulsant properties of methyl-beta-carboline-3-carboxylate (beta-CCM). The strain distribution patterns and estimates of the minimal number of loci obtained for each trait suggest that multiple chromosomal loci contribute to differences in anxiety-related behavioral phenotypes and the behavioral responses to diazepam and beta-CCM between C57BL/6J and A/J mice. The best probabilities of linkage were found between the variables characterizing response to diazepam and loci on chromosomes 1 (Xmv-41) and 10 (D10Mit2) and between the sensitivity to the convulsant actions of beta-CCM and locus D15Mit5 on chromosome 15."	Behav Genet	1995		"Mathis C, Neumann PE"	8540894	5 to 7 wks	both	9 to 20		10		62		26	30		30	20	42	U	15	U	32	30	U	20	32	17	U	28	30	20	U		70	18	U	20	10		15	U	60	40		U	33	60	10	72		U	U		U		U	U	U	5	33	85	
latency of the first seizure	sensitivity to convulsant properties if beta-CCM	Genetic analysis of anxiety-related behaviors and responses to benzodiazepine-related drugs in AXB and BXA recombinant inbred mouse strains.	"Recombinant inbred (RI) strains derived from the C57BL/6J and A/J mouse strains were used for behavioral studies designed to estimate the number and location of chromosomal loci responsible for anxiety-related behaviors and differential sensitivity to agonists and inverse agonists of the gamma-aminobutyric acidA (GABAA)/benzodiazepine receptor complex. The phenotypes of the parental inbred strains and of 28 RI strains were characterized for the number of transitions in the light<-->dark exploratory model, anxiolytic response to diazepam, vertical and ambulatory activities in an open field, and sensitivity to the convulsant properties of methyl-beta-carboline-3-carboxylate (beta-CCM). The strain distribution patterns and estimates of the minimal number of loci obtained for each trait suggest that multiple chromosomal loci contribute to differences in anxiety-related behavioral phenotypes and the behavioral responses to diazepam and beta-CCM between C57BL/6J and A/J mice. The best probabilities of linkage were found between the variables characterizing response to diazepam and loci on chromosomes 1 (Xmv-41) and 10 (D10Mit2) and between the sensitivity to the convulsant actions of beta-CCM and locus D15Mit5 on chromosome 15."	Behav Genet	1995		"Mathis C, Neumann PE"	8540894	5 to 7 wks 	both	10 to 20		200		850		900	800		480	600	800	U	900	U	570	300	U	300	200	200	U	720	300	400	U		720	800	U	900	650		500	U	800	900		U	900	900	570	90		U	U		U		U	U	U	720	30	800	
alcohol preference in males		Alcohol preference in AXB/BXA recombinant inbred mice: gender differences and gender-specific quantitative trait loci.	"The purpose of the present study was to characterize the C57BL/6J, A/J, and AXB/BXA Recombinant Inbred (RI) strains of mice for voluntary alcohol consumption. Quantitative Trait Locus (QTL) analysis was used to provide provisional location of QTLs for alcohol consumption. The inbred strains were screened for levels of alcohol intake (calculated as alcohol preference and absolute alcohol consumption) by receiving 4 days of forced exposure to a 10% (wt/vol) solution of alcohol, followed by 3 weeks of free choice between water and 10% alcohol. A wide and continuous distribution of values for alcohol consumption and preference was obtained in the AXB/BXA RI strains, confirming polygenic influences on alcohol-related behaviors. Significant gender differences were found for both alcohol preference [F28,651 = 2.12, p < 0.001] and absolute alcohol consumption [F28,647 = 2.57, p < 0.001]. In males, putative QTLs were mapped to chromosomes (Chrs) 2, 5, 7, 10, 11, and 16. Multiple regression analysis indicated that approximately 75% of the genetic variance in alcohol preference in males could be accounted for by three of the QTL regions. Several of the putative QTLs appeared to be male-specific (Tyr on Chr 7; D10Mit126 on Chr 10; D11Mit61 on Chr 11). In females, seven putative QTLs were mapped to Chrs 2, 4, 5, 7, 11, 16, and 19. Approximately 90% of the genetic variance in alcohol preference in females could be accounted for by four QTL regions, as determined by multiple regression. The QTL on Chr 11 near D11Mit35 appeared to be female-specific. This site was close to a female-specific QTL (Alcp2) previously mapped in C57BL/6J x DBA/2J backcrosses by Melo and coworkers (Nat Genet 13, 147, 1996). The QTLs mapped for alcohol preference in the present study must be considered suggestive at the present time, since only D2Mit74 met very strict statistical criteria for significance. However, the concordance across several studies for the loci on Chrs 2, 4, 7, 9, and 11 suggest that some common QTLs influencing alcohol preference have been identified. Confirmation of QTLs mapped in the present study is currently being conducted in a new series of recombinant congenic (RC) strains developed from reciprocal backcrosses between the A/J and C57BL/6J progenitors. The concomitant use of both RI and RC strains developed from the same progenitors should provide a powerful means of detecting, confirming, and mapping QTLs for alcohol-related traits."	Mamm Genome	1998		"Gill K, Desaulniers N"	9880655	8 wks 	both			0.18		0.53		0.35	0.23		0.25	0.2	0.33	U	0.25	U	0.35	0.2	0.35	0.4	U	0.33	U	0.2	0.2	0.18	U		U	0.15	U	U	0.6		0.45	U	0.2	0.2		U	0.2	0.26	0.6	0.22		0.45	0.15		U		U	U	U	0.43	0.2	U	
alcohol preference in females		Alcohol preference in AXB/BXA recombinant inbred mice: gender differences and gender-specific quantitative trait loci.	"The purpose of the present study was to characterize the C57BL/6J, A/J, and AXB/BXA Recombinant Inbred (RI) strains of mice for voluntary alcohol consumption. Quantitative Trait Locus (QTL) analysis was used to provide provisional location of QTLs for alcohol consumption. The inbred strains were screened for levels of alcohol intake (calculated as alcohol preference and absolute alcohol consumption) by receiving 4 days of forced exposure to a 10% (wt/vol) solution of alcohol, followed by 3 weeks of free choice between water and 10% alcohol. A wide and continuous distribution of values for alcohol consumption and preference was obtained in the AXB/BXA RI strains, confirming polygenic influences on alcohol-related behaviors. Significant gender differences were found for both alcohol preference [F28,651 = 2.12, p < 0.001] and absolute alcohol consumption [F28,647 = 2.57, p < 0.001]. In males, putative QTLs were mapped to chromosomes (Chrs) 2, 5, 7, 10, 11, and 16. Multiple regression analysis indicated that approximately 75% of the genetic variance in alcohol preference in males could be accounted for by three of the QTL regions. Several of the putative QTLs appeared to be male-specific (Tyr on Chr 7; D10Mit126 on Chr 10; D11Mit61 on Chr 11). In females, seven putative QTLs were mapped to Chrs 2, 4, 5, 7, 11, 16, and 19. Approximately 90% of the genetic variance in alcohol preference in females could be accounted for by four QTL regions, as determined by multiple regression. The QTL on Chr 11 near D11Mit35 appeared to be female-specific. This site was close to a female-specific QTL (Alcp2) previously mapped in C57BL/6J x DBA/2J backcrosses by Melo and coworkers (Nat Genet 13, 147, 1996). The QTLs mapped for alcohol preference in the present study must be considered suggestive at the present time, since only D2Mit74 met very strict statistical criteria for significance. However, the concordance across several studies for the loci on Chrs 2, 4, 7, 9, and 11 suggest that some common QTLs influencing alcohol preference have been identified. Confirmation of QTLs mapped in the present study is currently being conducted in a new series of recombinant congenic (RC) strains developed from reciprocal backcrosses between the A/J and C57BL/6J progenitors. The concomitant use of both RI and RC strains developed from the same progenitors should provide a powerful means of detecting, confirming, and mapping QTLs for alcohol-related traits."	Mamm Genome	1998		"Gill K, Desaulniers N"	9880655	8 wks 	both			0.28		0.55		0.5	0.47		0.3	0.2	0.32	U	0.35	U	0.26	0.23	0.4	0.28	U	0.28	U	0.22	0.28	0.27	U		U	0.17	U	U	0.55		0.33	U	0.3	0.26		U	0.33	0.45	0.6	0.4		0.5	0.15		U		U	U	U	0.38	0.27	U	
alcohol consumption in males		Alcohol preference in AXB/BXA recombinant inbred mice: gender differences and gender-specific quantitative trait loci.	"The purpose of the present study was to characterize the C57BL/6J, A/J, and AXB/BXA Recombinant Inbred (RI) strains of mice for voluntary alcohol consumption. Quantitative Trait Locus (QTL) analysis was used to provide provisional location of QTLs for alcohol consumption. The inbred strains were screened for levels of alcohol intake (calculated as alcohol preference and absolute alcohol consumption) by receiving 4 days of forced exposure to a 10% (wt/vol) solution of alcohol, followed by 3 weeks of free choice between water and 10% alcohol. A wide and continuous distribution of values for alcohol consumption and preference was obtained in the AXB/BXA RI strains, confirming polygenic influences on alcohol-related behaviors. Significant gender differences were found for both alcohol preference [F28,651 = 2.12, p < 0.001] and absolute alcohol consumption [F28,647 = 2.57, p < 0.001]. In males, putative QTLs were mapped to chromosomes (Chrs) 2, 5, 7, 10, 11, and 16. Multiple regression analysis indicated that approximately 75% of the genetic variance in alcohol preference in males could be accounted for by three of the QTL regions. Several of the putative QTLs appeared to be male-specific (Tyr on Chr 7; D10Mit126 on Chr 10; D11Mit61 on Chr 11). In females, seven putative QTLs were mapped to Chrs 2, 4, 5, 7, 11, 16, and 19. Approximately 90% of the genetic variance in alcohol preference in females could be accounted for by four QTL regions, as determined by multiple regression. The QTL on Chr 11 near D11Mit35 appeared to be female-specific. This site was close to a female-specific QTL (Alcp2) previously mapped in C57BL/6J x DBA/2J backcrosses by Melo and coworkers (Nat Genet 13, 147, 1996). The QTLs mapped for alcohol preference in the present study must be considered suggestive at the present time, since only D2Mit74 met very strict statistical criteria for significance. However, the concordance across several studies for the loci on Chrs 2, 4, 7, 9, and 11 suggest that some common QTLs influencing alcohol preference have been identified. Confirmation of QTLs mapped in the present study is currently being conducted in a new series of recombinant congenic (RC) strains developed from reciprocal backcrosses between the A/J and C57BL/6J progenitors. The concomitant use of both RI and RC strains developed from the same progenitors should provide a powerful means of detecting, confirming, and mapping QTLs for alcohol-related traits."	Mamm Genome	1998		"Gill K, Desaulniers N"	9880655	8 wks 	both		g/kg/day	3.5		10		8.5	4.5		8.5	4.5	9.5	U	6.5	U	3.5	5.5	6.5	10.5	U	10	U	4.5	4.5	3.7	U		U	5	U	U	10		9	U	5.5	3		U	5.5	6	15	4.5		11	3		U		U	U	U	8.5	5	U	
alcohol consumption in females		Alcohol preference in AXB/BXA recombinant inbred mice: gender differences and gender-specific quantitative trait loci.	"The purpose of the present study was to characterize the C57BL/6J, A/J, and AXB/BXA Recombinant Inbred (RI) strains of mice for voluntary alcohol consumption. Quantitative Trait Locus (QTL) analysis was used to provide provisional location of QTLs for alcohol consumption. The inbred strains were screened for levels of alcohol intake (calculated as alcohol preference and absolute alcohol consumption) by receiving 4 days of forced exposure to a 10% (wt/vol) solution of alcohol, followed by 3 weeks of free choice between water and 10% alcohol. A wide and continuous distribution of values for alcohol consumption and preference was obtained in the AXB/BXA RI strains, confirming polygenic influences on alcohol-related behaviors. Significant gender differences were found for both alcohol preference [F28,651 = 2.12, p < 0.001] and absolute alcohol consumption [F28,647 = 2.57, p < 0.001]. In males, putative QTLs were mapped to chromosomes (Chrs) 2, 5, 7, 10, 11, and 16. Multiple regression analysis indicated that approximately 75% of the genetic variance in alcohol preference in males could be accounted for by three of the QTL regions. Several of the putative QTLs appeared to be male-specific (Tyr on Chr 7; D10Mit126 on Chr 10; D11Mit61 on Chr 11). In females, seven putative QTLs were mapped to Chrs 2, 4, 5, 7, 11, 16, and 19. Approximately 90% of the genetic variance in alcohol preference in females could be accounted for by four QTL regions, as determined by multiple regression. The QTL on Chr 11 near D11Mit35 appeared to be female-specific. This site was close to a female-specific QTL (Alcp2) previously mapped in C57BL/6J x DBA/2J backcrosses by Melo and coworkers (Nat Genet 13, 147, 1996). The QTLs mapped for alcohol preference in the present study must be considered suggestive at the present time, since only D2Mit74 met very strict statistical criteria for significance. However, the concordance across several studies for the loci on Chrs 2, 4, 7, 9, and 11 suggest that some common QTLs influencing alcohol preference have been identified. Confirmation of QTLs mapped in the present study is currently being conducted in a new series of recombinant congenic (RC) strains developed from reciprocal backcrosses between the A/J and C57BL/6J progenitors. The concomitant use of both RI and RC strains developed from the same progenitors should provide a powerful means of detecting, confirming, and mapping QTLs for alcohol-related traits."	Mamm Genome	1998		"Gill K, Desaulniers N"	9880655	8 wks 	both		g/kg/day	8		14		16	17		10	6	10	U	9	U	8	6	8.5	9	U	7.5	U	6.5	6.5	6	U		U	6	U	U	12		9	U	9	5.5		U	6.5	14	18	9		14	4		U		U	U	U	9	6	U	
brain weight		"Eye1 and Eye2: gene loci that modulate eye size, lens weight, and retinal area in the mouse."	"PURPOSE: Vision is critically dependent on genetic factors that influence the rate and duration of eye growth. The genetic basis of variation in eye size in mice was explored, and genes that modulate eye weight, lens weight, and retinal area were mapped. METHODS: Eyes of approximately 700 mice were weighed. Data were corrected by regression analysis to eliminate effects of sex, age, and body weight. Interval mapping was used to locate quantitative trait loci (QTLs) using recombinant inbred strains and F2 intercrosses between strains C57BL/6J and DBA/2J. RESULTS: Major QTLs were discovered near the centromere of chromosome 5 (Eye1: genomewide P E 0.005) and on proximal chromosome 17 near the mast cell protease 6 gene (Eye2, P ] 0.05). Both QTLs have significant effects on eye size, lens weight, and retinal area. The DBA/2J alleles at Eye1 and Eye2 are partially dominant and increase eye weight by as much as 1.0 mg. Analysis of 183 F2 progeny confirmed and refined the chromosomal assignments of both Eye1 and Eye2. CONCLUSIONS: Eye1 and Eye2 are the first loci known to control normal variation in eye size in any mammal. The hepatic growth factor gene (Hgf), a potent mitogen expressed in the retina, pigment epithelium, and choroid, is a strong candidate for Eye1. The human homolog of Eye2 should map to chromosome 6p, 16q13.3, or 19q13, whereas that of Eye1 should map to 7q."	Invest Ophthalmol Vis Sci	1999		"Zhou G, Williams RW"	10102277	100 days	both		mg	U		U		405.2	456.6		412.2	443	462	U	413.6	U	457	U	398	436.4	U	413.2	U	434.6	450	435.8	U		U	418.5	U	430.6	438.4		398	U	446.1	424.8		U	449.5	434.7	438.2	406.8		417	449.1		U		U	U	U	424	468.9	409.4	Nathan Copeland
body weight		"Eye1 and Eye2: gene loci that modulate eye size, lens weight, and retinal area in the mouse."	"PURPOSE: Vision is critically dependent on genetic factors that influence the rate and duration of eye growth. The genetic basis of variation in eye size in mice was explored, and genes that modulate eye weight, lens weight, and retinal area were mapped. METHODS: Eyes of approximately 700 mice were weighed. Data were corrected by regression analysis to eliminate effects of sex, age, and body weight. Interval mapping was used to locate quantitative trait loci (QTLs) using recombinant inbred strains and F2 intercrosses between strains C57BL/6J and DBA/2J. RESULTS: Major QTLs were discovered near the centromere of chromosome 5 (Eye1: genomewide P E 0.005) and on proximal chromosome 17 near the mast cell protease 6 gene (Eye2, P ] 0.05). Both QTLs have significant effects on eye size, lens weight, and retinal area. The DBA/2J alleles at Eye1 and Eye2 are partially dominant and increase eye weight by as much as 1.0 mg. Analysis of 183 F2 progeny confirmed and refined the chromosomal assignments of both Eye1 and Eye2. CONCLUSIONS: Eye1 and Eye2 are the first loci known to control normal variation in eye size in any mammal. The hepatic growth factor gene (Hgf), a potent mitogen expressed in the retina, pigment epithelium, and choroid, is a strong candidate for Eye1. The human homolog of Eye2 should map to chromosome 6p, 16q13.3, or 19q13, whereas that of Eye1 should map to 7q."	Invest Ophthalmol Vis Sci	1999		"Zhou G, Williams RW"	10102277	100 days	both		g	U		U		18.6	21.2		17.1	19.8	22.8	U	17.6	U	20.3	U	19.8	20.6	U	18.9	U	18.5	20.1	18.4	U		U	19.3	U	19.7	19.9		19.1	U	21.5	20.5		U	20.5	16	17.4	22.7		19.1	20.6		U		U	U	U	20.7	23.3	18.9	Nathan Copeland
olfactory bulb weight									100 days	both			U		U		20.5	22		20	22.7	23.6	U	19.7	U	22.9	U	18.4	U	U	20.8	U	21.3	22.9	20.3	U		U	20.9	U	20.3	22.2		21.3	U	22.9	21		U	23.3	20.6	22.5	19.2		20.6	20.1		U		U	U	U	19.7	22.4	19.5	
cerebellum weight									100 days	both			U		U		54.8	61.5		52.3	60.7	57.8	U	49.7	U	61	U	48.6	U	U	51.7	U	53.9	57.9	57	U		U	57.3	U	51.8	61.7		54.7	U	60.9	55.8		U	63.4	53.1	59.4	58.1		54.4	55.6		U		U	U	U	58	68.9	51	
hippocampus weight									100 days	both			U		U		25.6	28.5		U	26	26.9	U	23.8	U	25.7	U	22.3	U	U	26.3	U	25.2	26	25.6	U		U	23.8	U	23.6	27.2		23.6	U	25.6	25.9		U	26.3	26.3	27.4	23.5		24.8	U		U		U	U	U	24.4	U	23.6	
forebrain plus mid weight									100 days	both			U		U		289.7	330.6		291.7	327	329.3	U	294.8	U	319.4	U	292.8	U	U	304	U	322.5	327.1	306.6	U		U	305	U	307.2	310.4		283.5	U	318.2	313.8		U	325.4	319.7	321.3	298.3		299.5	323.8		U		U	U	U	303.5	332.8	294.7	
Lung PKC- a activity and content AxB and BxA strains relative to A/J strain	PKC-  a Content	Quantitative trait locus mapping of genes regulating pulmonary PKC activity and PKC-alpha content.	"Strain A/J mice, which are predisposed to experimentally induced asthma and adenocarcinoma, have the lowest pulmonary protein kinase (PK) C activity and content among 22 inbred mouse strains. PKC in neonatal A/J mice is similar to that in other strains, so this difference reflects strain-dependent postnatal regulation. PKC activity is 60% higher in C57BL/6J (B6) than in A/J lungs, and the protein and mRNA concentrations of PKC-alpha, the major pulmonary PKC isozyme, are two- to threefold higher in B6 mice. These differences result from more than a single gene as assessed in F(1), F(2), and backcross progeny of B6 and A/J parents. Quantitative trait locus (QTL) analysis of 23 AxB and BxA recombinant inbred strains derived from B6 and A/J progenitors indicates a major locus regulating lung PKC-alpha content that maps near the Pkcalpha structural gene on chromosome 11 (D11MIT333; likelihood ratio statistic = 12.5) and a major locus controlling PKC activity that maps on chromosome 3 (D3MIT19; likelihood ratio statistic = 15.4). The chromosome 11 QTL responsible for low PKC-alpha content falls within QTLs for susceptibilities to lung tumorigenesis and ozone-induced toxicity."	AJP - Lung Cellular and molecular Physiology	2000	Aug	"Lori D. Dwyer-Nield, Beverly Paigen, Stephanie E. Porter, and Alvin M. Malkinson"	10926556	42 - 98 days	both	6-Mar	strains relative to A/J strain	---		---		1.1 0.2	1.7		4.2	1.1	0.8	---	6	---	3.7	0.9	---	0.7	---	8.8	---	0.7	1.1	ND	---		0.9	0.8	---	---	2.8		7.7	---	---	---		---	ND	6.7	ND	---		---	---		---		---	---	---	5.8	1.3	2.1	Nathan Copeland
Lung PKC- a activity and content AxB and BxA strains relative to A/J strain	PKC Activity	Quantitative trait locus mapping of genes regulating pulmonary PKC activity and PKC-alpha content.	"Strain A/J mice, which are predisposed to experimentally induced asthma and adenocarcinoma, have the lowest pulmonary protein kinase (PK) C activity and content among 22 inbred mouse strains. PKC in neonatal A/J mice is similar to that in other strains, so this difference reflects strain-dependent postnatal regulation. PKC activity is 60% higher in C57BL/6J (B6) than in A/J lungs, and the protein and mRNA concentrations of PKC-alpha, the major pulmonary PKC isozyme, are two- to threefold higher in B6 mice. These differences result from more than a single gene as assessed in F(1), F(2), and backcross progeny of B6 and A/J parents. Quantitative trait locus (QTL) analysis of 23 AxB and BxA recombinant inbred strains derived from B6 and A/J progenitors indicates a major locus regulating lung PKC-alpha content that maps near the Pkcalpha structural gene on chromosome 11 (D11MIT333; likelihood ratio statistic = 12.5) and a major locus controlling PKC activity that maps on chromosome 3 (D3MIT19; likelihood ratio statistic = 15.4). The chromosome 11 QTL responsible for low PKC-alpha content falls within QTLs for susceptibilities to lung tumorigenesis and ozone-induced toxicity."	AJP - Lung Cellular and molecular Physiology	2000	Aug	"Lori D. Dwyer-Nield, Beverly Paigen, Stephanie E. Porter, and Alvin M. Malkinson"	10926556	42 - 98 days	both	6-Mar	strains relative to A/J strain	---		---		1	ND		1.5	0.8	ND	---	1.6	---	0.9	ND	---	1	---	2.7	---	1	1.1	1.4	---		1	ND	---	---	1.5		ND	---	---	---		---	1.5	2.1	2.1	---		---	---		---		---	---	---	1.2	0.8	ND	Nathan Copeland
hepatic inflammation	area on inflammation per portal area	Differential susceptibility to hepatic inflammation and proliferation in AXB recombinant inbred mice chronically infected with Helicobacter hepaticus.	"Helicobacter hepaticus is a naturally occurring pathogen of mice and has been used to develop models of chronic hepatitis, liver cancer, and, more recently, inflammatory bowel disease, in selected mouse strains. A/JCr mice are particularly susceptible to H. hepaticus-induced hepatitis and subsequent development of liver neoplasms, whereas C57BL/6 mice are resistant. In this study, we inoculated nine AXB recombinant inbred (RI) mouse strains, derived from A/J and C57BL/6 mice, with H. hepaticus to determine the genetic basis of resistance to Helicobacter-induced liver disease. Mice were surveyed 14 months after inoculation by culture and PCR for H. hepaticus colonization of the liver and cecum, and microscopic morphometric evaluations of the liver were performed to quantify and correlate the severity of inflammation, apoptosis, and proliferation. Analysis of variance of hepatic inflammation demonstrated significant variation among the RI strains (P < 0.0001), and the strain distribution pattern suggested a multigenic basis of disease resistance. Quantitative trait analysis using linear regression suggested possible linkage to loci on mouse chromosome 19. Hepatocellular and biliary epithelial apoptosis and proliferation indices, including proliferation of oval cells, were markedly increased and correlated with severity of inflammation. Prevalence of hepatic neoplasia was also increased in susceptible RI strains. These findings demonstrate a genetic basis for susceptibility to Helicobacter-induced disease and provide insight into its pathogenesis."	Am J Pathol	1999	Aug	"Ihrig M, Schrenzel MD, Fox JG"	1043349	adult	both	10	square microns	---		---		5000	2500		600	1400	2300	---	5100	---	2800	---	3100	1100	---	---	---	---	---	---	---		---	---	---																										
Hepatic PMN infiltration phenotypes of AXB/BXA RI strains		Quantitative trait loci modulate neutrophil infiltration in the liver during LPS-induced inflammation.	"A crucial aspect of the inflammatory response is the recruitment of activated neutrophils (PMN) to the site of damage. Lytic enzymes and oxygen radicals released by PMN are important in clearing an infection or cellular debris, but can also produce host tissue damage. Failure to properly regulate the inflammatory response contributes to a variety of human diseases like sepsis and multiple organ dysfunction syndrome, the leading cause of morbidity and mortality in surgical intensive care units. Many aspects of human disease pathology, including hepatic PMN infiltration, can be recapitulated in mice using an endotoxic shock model. Six quantitative trait loci that predispose to high infiltration of PMN in hepatic sinusoids after high-dose endotoxin administration were provisionally identified. Two of these loci, Hpi1 and Hpi2 on mouse chromosomes 5 and 13, were mapped to the significant and highly significant level using a low-resolution genome scan on 122 intercross animals. These loci interact epistatically to produce a high degree of PMN infiltration. Intercross and recombinant inbred strain mice with a specific genotype at these loci always had a high infiltration response, indicating that genotype analysis at just these two loci can accurately predict a high PMN infiltration response. Genetic predisposition to the degree of PMN infiltration in the inflammatory response in mice suggests that analogous genetic mechanisms occur in human beings that could be used for diagnostic purposes."	FASEB J	2000	Nov	"Matesic LE, Niemitz EL, De Maio A, Reeves RH."	11053246	8- 9 wks	male	3	average number PMN/ high power hepatic field	15		51		43	40		47	31	55		31		62		46	43		50		36	38	23				34		64	45		35		82	34			51	32	32	68		50	45							37	38	19	Nathan Copeland
Strain distribution pattern in RI lines in relationship to Ucpl mRNA levels	Chromosome 8: 8M128:  31 cM	Synergistic gene interactions control the induction of the mitochondrial uncoupling protein (Ucp1) gene in white fat tissue.	"Among a selected group of mouse strains susceptible to dietary obesity, those with an enhanced capacity for Ucp1 and brown adipocyte induction in white fat preferentially lost body weight following adrenergic stimulation. Based on the generality of this mechanism for reducing obesity, a genetic analysis was initiated to identify genes that control brown adipocyte induction in white fat depots in mice. Quantitative trait locus (QTL) analysis was performed using the variations of retroperitoneal fat Ucp1 mRNA expression in progeny of genetic crosses between the A/J and C57BL/6J parental strains and selected AXB recombinant inbred strains. Three A/J-derived loci on chromosomes 2, 3, and 8 and one C57BL/6J locus on chromosome 19 were linked to Ucp1 induction in retroperitoneal fat. Although A/J-derived alleles seemed to contribute to elevated Ucp1 expression, the C57BL/6J allele on chromosome 19 increased Ucp1 mRNA to levels higher than parental values. Thus, novel patterns of C57BL/6J and A/J recombinant genotypes among the four mapped loci resulted in a transgressive variation of Ucp1 phenotypes. Although the extent of the interchromosomal interactions have not been fully explored, strong synergistic interactions occur between a C57BL/6J allele on chromosome 19 and an A/J allele on chromosome 8. In addition to selective synergistic interactions between loci, variations in recessive and dominant effects also contribute to the final levels of Ucp1 expression."	J Biol Chem	2000	Nov	"Koza RA, Hohmann SM, Guerra C, Rossmeisl M, Kozak"	109831824	2-3 months	male			A		B		B	A		A	B	B		A		B		B		A	A		A	A	A				B		B	B		A		B	B			B	A	B	A			B							B	A		Nathan Copeland
Strain distribution pattern in RI lines in relationship to Ucpl mRNA levels	Chromosome 8:8M31:  34 cM	Synergistic gene interactions control the induction of the mitochondrial uncoupling protein (Ucp1) gene in white fat tissue.	"Among a selected group of mouse strains susceptible to dietary obesity, those with an enhanced capacity for Ucp1 and brown adipocyte induction in white fat preferentially lost body weight following adrenergic stimulation. Based on the generality of this mechanism for reducing obesity, a genetic analysis was initiated to identify genes that control brown adipocyte induction in white fat depots in mice. Quantitative trait locus (QTL) analysis was performed using the variations of retroperitoneal fat Ucp1 mRNA expression in progeny of genetic crosses between the A/J and C57BL/6J parental strains and selected AXB recombinant inbred strains. Three A/J-derived loci on chromosomes 2, 3, and 8 and one C57BL/6J locus on chromosome 19 were linked to Ucp1 induction in retroperitoneal fat. Although A/J-derived alleles seemed to contribute to elevated Ucp1 expression, the C57BL/6J allele on chromosome 19 increased Ucp1 mRNA to levels higher than parental values. Thus, novel patterns of C57BL/6J and A/J recombinant genotypes among the four mapped loci resulted in a transgressive variation of Ucp1 phenotypes. Although the extent of the interchromosomal interactions have not been fully explored, strong synergistic interactions occur between a C57BL/6J allele on chromosome 19 and an A/J allele on chromosome 8. In addition to selective synergistic interactions between loci, variations in recessive and dominant effects also contribute to the final levels of Ucp1 expression."	J Biol Chem	2000	Nov	"Koza RA, Hohmann SM, Guerra C, Rossmeisl M, Kozak"	109831824	2-3 months	male			A		B		B	B		A	B	B		A		B		B		A	A		A	A	A				B		B	B		A		B	B			B	A	B	A			A							B	A		Nathan Copeland
Strain distribution pattern in RI lines in relationship to Ucpl mRNA levels	Chromosome 8:Ucp1:  37.7 cM	Synergistic gene interactions control the induction of the mitochondrial uncoupling protein (Ucp1) gene in white fat tissue.	"Among a selected group of mouse strains susceptible to dietary obesity, those with an enhanced capacity for Ucp1 and brown adipocyte induction in white fat preferentially lost body weight following adrenergic stimulation. Based on the generality of this mechanism for reducing obesity, a genetic analysis was initiated to identify genes that control brown adipocyte induction in white fat depots in mice. Quantitative trait locus (QTL) analysis was performed using the variations of retroperitoneal fat Ucp1 mRNA expression in progeny of genetic crosses between the A/J and C57BL/6J parental strains and selected AXB recombinant inbred strains. Three A/J-derived loci on chromosomes 2, 3, and 8 and one C57BL/6J locus on chromosome 19 were linked to Ucp1 induction in retroperitoneal fat. Although A/J-derived alleles seemed to contribute to elevated Ucp1 expression, the C57BL/6J allele on chromosome 19 increased Ucp1 mRNA to levels higher than parental values. Thus, novel patterns of C57BL/6J and A/J recombinant genotypes among the four mapped loci resulted in a transgressive variation of Ucp1 phenotypes. Although the extent of the interchromosomal interactions have not been fully explored, strong synergistic interactions occur between a C57BL/6J allele on chromosome 19 and an A/J allele on chromosome 8. In addition to selective synergistic interactions between loci, variations in recessive and dominant effects also contribute to the final levels of Ucp1 expression."	J Biol Chem	2000	Nov	"Koza RA, Hohmann SM, Guerra C, Rossmeisl M, Kozak"	109831824	2-3 months	male			A		B		B	B		A	B	B		A		B		B		A	A		A	A	A				A		B	A		A		B	A			A	A	B	A			A							B	A		Nathan Copeland
Strain distribution pattern in RI lines in relationship to Ucpl mRNA levels	Chromosome 8:8M45:  40.5 cM	Synergistic gene interactions control the induction of the mitochondrial uncoupling protein (Ucp1) gene in white fat tissue.	"Among a selected group of mouse strains susceptible to dietary obesity, those with an enhanced capacity for Ucp1 and brown adipocyte induction in white fat preferentially lost body weight following adrenergic stimulation. Based on the generality of this mechanism for reducing obesity, a genetic analysis was initiated to identify genes that control brown adipocyte induction in white fat depots in mice. Quantitative trait locus (QTL) analysis was performed using the variations of retroperitoneal fat Ucp1 mRNA expression in progeny of genetic crosses between the A/J and C57BL/6J parental strains and selected AXB recombinant inbred strains. Three A/J-derived loci on chromosomes 2, 3, and 8 and one C57BL/6J locus on chromosome 19 were linked to Ucp1 induction in retroperitoneal fat. Although A/J-derived alleles seemed to contribute to elevated Ucp1 expression, the C57BL/6J allele on chromosome 19 increased Ucp1 mRNA to levels higher than parental values. Thus, novel patterns of C57BL/6J and A/J recombinant genotypes among the four mapped loci resulted in a transgressive variation of Ucp1 phenotypes. Although the extent of the interchromosomal interactions have not been fully explored, strong synergistic interactions occur between a C57BL/6J allele on chromosome 19 and an A/J allele on chromosome 8. In addition to selective synergistic interactions between loci, variations in recessive and dominant effects also contribute to the final levels of Ucp1 expression."	J Biol Chem	2000	Nov	"Koza RA, Hohmann SM, Guerra C, Rossmeisl M, Kozak"	109831824	2-3 months	male			A		B		B	A		A	B	B		A		B		B		A	A		A	A	A				A		B	A		A		B	A			A	A	B	A			A							B	A		Nathan Copeland
Strain distribution pattern in RI lines in relationship to Ucpl mRNA levels	Chromosome 8:8M242:  47 cM	Synergistic gene interactions control the induction of the mitochondrial uncoupling protein (Ucp1) gene in white fat tissue.	"Among a selected group of mouse strains susceptible to dietary obesity, those with an enhanced capacity for Ucp1 and brown adipocyte induction in white fat preferentially lost body weight following adrenergic stimulation. Based on the generality of this mechanism for reducing obesity, a genetic analysis was initiated to identify genes that control brown adipocyte induction in white fat depots in mice. Quantitative trait locus (QTL) analysis was performed using the variations of retroperitoneal fat Ucp1 mRNA expression in progeny of genetic crosses between the A/J and C57BL/6J parental strains and selected AXB recombinant inbred strains. Three A/J-derived loci on chromosomes 2, 3, and 8 and one C57BL/6J locus on chromosome 19 were linked to Ucp1 induction in retroperitoneal fat. Although A/J-derived alleles seemed to contribute to elevated Ucp1 expression, the C57BL/6J allele on chromosome 19 increased Ucp1 mRNA to levels higher than parental values. Thus, novel patterns of C57BL/6J and A/J recombinant genotypes among the four mapped loci resulted in a transgressive variation of Ucp1 phenotypes. Although the extent of the interchromosomal interactions have not been fully explored, strong synergistic interactions occur between a C57BL/6J allele on chromosome 19 and an A/J allele on chromosome 8. In addition to selective synergistic interactions between loci, variations in recessive and dominant effects also contribute to the final levels of Ucp1 expression."	J Biol Chem	2000	Nov	"Koza RA, Hohmann SM, Guerra C, Rossmeisl M, Kozak"	109831824	2-3 months	male			A		B		A	A		A	B	B		A		A		B		A	A		A	A	A				A		B	A		B		B	A			A	A	B	B			A							B	B		Nathan Copeland
Strain distribution pattern in RI lines in relationship to Ucpl mRNA levels	RP Ucp1---mRNA	Synergistic gene interactions control the induction of the mitochondrial uncoupling protein (Ucp1) gene in white fat tissue.	"Among a selected group of mouse strains susceptible to dietary obesity, those with an enhanced capacity for Ucp1 and brown adipocyte induction in white fat preferentially lost body weight following adrenergic stimulation. Based on the generality of this mechanism for reducing obesity, a genetic analysis was initiated to identify genes that control brown adipocyte induction in white fat depots in mice. Quantitative trait locus (QTL) analysis was performed using the variations of retroperitoneal fat Ucp1 mRNA expression in progeny of genetic crosses between the A/J and C57BL/6J parental strains and selected AXB recombinant inbred strains. Three A/J-derived loci on chromosomes 2, 3, and 8 and one C57BL/6J locus on chromosome 19 were linked to Ucp1 induction in retroperitoneal fat. Although A/J-derived alleles seemed to contribute to elevated Ucp1 expression, the C57BL/6J allele on chromosome 19 increased Ucp1 mRNA to levels higher than parental values. Thus, novel patterns of C57BL/6J and A/J recombinant genotypes among the four mapped loci resulted in a transgressive variation of Ucp1 phenotypes. Although the extent of the interchromosomal interactions have not been fully explored, strong synergistic interactions occur between a C57BL/6J allele on chromosome 19 and an A/J allele on chromosome 8. In addition to selective synergistic interactions between loci, variations in recessive and dominant effects also contribute to the final levels of Ucp1 expression."	J Biol Chem	2000	Nov	"Koza RA, Hohmann SM, Guerra C, Rossmeisl M, Kozak"	109831824	2-3 months	male			668		16		40	77		1700	153	226		1717		13		122		1247	1490		630	1181	896				562		37	51		359		86	186			387	295	51	1439			200							55	576		Nathan Copeland
Strain distribution pattern in RI lines in relationship to Ucpl mRNA levels	Chromosome 19:  19M106:   18.5cM	Synergistic gene interactions control the induction of the mitochondrial uncoupling protein (Ucp1) gene in white fat tissue.	"Among a selected group of mouse strains susceptible to dietary obesity, those with an enhanced capacity for Ucp1 and brown adipocyte induction in white fat preferentially lost body weight following adrenergic stimulation. Based on the generality of this mechanism for reducing obesity, a genetic analysis was initiated to identify genes that control brown adipocyte induction in white fat depots in mice. Quantitative trait locus (QTL) analysis was performed using the variations of retroperitoneal fat Ucp1 mRNA expression in progeny of genetic crosses between the A/J and C57BL/6J parental strains and selected AXB recombinant inbred strains. Three A/J-derived loci on chromosomes 2, 3, and 8 and one C57BL/6J locus on chromosome 19 were linked to Ucp1 induction in retroperitoneal fat. Although A/J-derived alleles seemed to contribute to elevated Ucp1 expression, the C57BL/6J allele on chromosome 19 increased Ucp1 mRNA to levels higher than parental values. Thus, novel patterns of C57BL/6J and A/J recombinant genotypes among the four mapped loci resulted in a transgressive variation of Ucp1 phenotypes. Although the extent of the interchromosomal interactions have not been fully explored, strong synergistic interactions occur between a C57BL/6J allele on chromosome 19 and an A/J allele on chromosome 8. In addition to selective synergistic interactions between loci, variations in recessive and dominant effects also contribute to the final levels of Ucp1 expression."	J Biol Chem	2000	Nov	"Koza RA, Hohmann SM, Guerra C, Rossmeisl M, Kozak"	109831824	2-3 months	male			A		B		B	A		B	B	A		B		B		A		B	B		B	B	B				B		B	A		A		A	B			A	B	A	B			B							A	B		Nathan Copeland
Strain distribution pattern in RI lines in relationship to Ucpl mRNA levels	Chromosome 19:   19M86:   20 cM	Synergistic gene interactions control the induction of the mitochondrial uncoupling protein (Ucp1) gene in white fat tissue.	"Among a selected group of mouse strains susceptible to dietary obesity, those with an enhanced capacity for Ucp1 and brown adipocyte induction in white fat preferentially lost body weight following adrenergic stimulation. Based on the generality of this mechanism for reducing obesity, a genetic analysis was initiated to identify genes that control brown adipocyte induction in white fat depots in mice. Quantitative trait locus (QTL) analysis was performed using the variations of retroperitoneal fat Ucp1 mRNA expression in progeny of genetic crosses between the A/J and C57BL/6J parental strains and selected AXB recombinant inbred strains. Three A/J-derived loci on chromosomes 2, 3, and 8 and one C57BL/6J locus on chromosome 19 were linked to Ucp1 induction in retroperitoneal fat. Although A/J-derived alleles seemed to contribute to elevated Ucp1 expression, the C57BL/6J allele on chromosome 19 increased Ucp1 mRNA to levels higher than parental values. Thus, novel patterns of C57BL/6J and A/J recombinant genotypes among the four mapped loci resulted in a transgressive variation of Ucp1 phenotypes. Although the extent of the interchromosomal interactions have not been fully explored, strong synergistic interactions occur between a C57BL/6J allele on chromosome 19 and an A/J allele on chromosome 8. In addition to selective synergistic interactions between loci, variations in recessive and dominant effects also contribute to the final levels of Ucp1 expression."	J Biol Chem	2000	Nov	"Koza RA, Hohmann SM, Guerra C, Rossmeisl M, Kozak"	109831824	2-3 months	male			A		B		B	A		B	B	A		B		A		A		B	B		B	B	B				B		B	A		B		A	B			A	B	A	B			B							A	B		Nathan Copeland
Strain distribution pattern in RI lines in relationship to Ucpl mRNA levels	Chromosome 19:   19M99:   20.3 cM	Synergistic gene interactions control the induction of the mitochondrial uncoupling protein (Ucp1) gene in white fat tissue.	"Among a selected group of mouse strains susceptible to dietary obesity, those with an enhanced capacity for Ucp1 and brown adipocyte induction in white fat preferentially lost body weight following adrenergic stimulation. Based on the generality of this mechanism for reducing obesity, a genetic analysis was initiated to identify genes that control brown adipocyte induction in white fat depots in mice. Quantitative trait locus (QTL) analysis was performed using the variations of retroperitoneal fat Ucp1 mRNA expression in progeny of genetic crosses between the A/J and C57BL/6J parental strains and selected AXB recombinant inbred strains. Three A/J-derived loci on chromosomes 2, 3, and 8 and one C57BL/6J locus on chromosome 19 were linked to Ucp1 induction in retroperitoneal fat. Although A/J-derived alleles seemed to contribute to elevated Ucp1 expression, the C57BL/6J allele on chromosome 19 increased Ucp1 mRNA to levels higher than parental values. Thus, novel patterns of C57BL/6J and A/J recombinant genotypes among the four mapped loci resulted in a transgressive variation of Ucp1 phenotypes. Although the extent of the interchromosomal interactions have not been fully explored, strong synergistic interactions occur between a C57BL/6J allele on chromosome 19 and an A/J allele on chromosome 8. In addition to selective synergistic interactions between loci, variations in recessive and dominant effects also contribute to the final levels of Ucp1 expression."	J Biol Chem	2000	Nov	"Koza RA, Hohmann SM, Guerra C, Rossmeisl M, Kozak"	109831824	2-3 months	male			A		B		B	A		B	B	A		B		A		A		A	B		B	B	B				B		B	A		B		A	B			A	B	A	B			B							A	B		Nathan Copeland
Strain distribution pattern in RI lines in relationship to Ucpl mRNA levels	Chromosome 19:   19M30:   21.4 cM	Synergistic gene interactions control the induction of the mitochondrial uncoupling protein (Ucp1) gene in white fat tissue.	"Among a selected group of mouse strains susceptible to dietary obesity, those with an enhanced capacity for Ucp1 and brown adipocyte induction in white fat preferentially lost body weight following adrenergic stimulation. Based on the generality of this mechanism for reducing obesity, a genetic analysis was initiated to identify genes that control brown adipocyte induction in white fat depots in mice. Quantitative trait locus (QTL) analysis was performed using the variations of retroperitoneal fat Ucp1 mRNA expression in progeny of genetic crosses between the A/J and C57BL/6J parental strains and selected AXB recombinant inbred strains. Three A/J-derived loci on chromosomes 2, 3, and 8 and one C57BL/6J locus on chromosome 19 were linked to Ucp1 induction in retroperitoneal fat. Although A/J-derived alleles seemed to contribute to elevated Ucp1 expression, the C57BL/6J allele on chromosome 19 increased Ucp1 mRNA to levels higher than parental values. Thus, novel patterns of C57BL/6J and A/J recombinant genotypes among the four mapped loci resulted in a transgressive variation of Ucp1 phenotypes. Although the extent of the interchromosomal interactions have not been fully explored, strong synergistic interactions occur between a C57BL/6J allele on chromosome 19 and an A/J allele on chromosome 8. In addition to selective synergistic interactions between loci, variations in recessive and dominant effects also contribute to the final levels of Ucp1 expression."	J Biol Chem	2000	Nov	"Koza RA, Hohmann SM, Guerra C, Rossmeisl M, Kozak"	109831824	2-3 months	male			A		B		B	B		B	B	A		B		A		B		A	B		B	B	B				B		B	A		B		A	B			A	B	A	B			B							A	B		Nathan Copeland
"Mammary patterning phenotypes of A/J, C57BL/6, and 30 AXB/BXA recombinant inbred strains"	Number of ska MG pattern phenotypes - percent of total	Mammary gland patterning in the AXB/BXA recombinant inbred strains of mouse.		Mech Dev	2000	Mar	"Howard BA, Gusterson BA"	10704854		female	Feb-75		40 - 0.95		0 - 0.00		8 - 0.89	10 - 1.00		9 - 1.00	0 - 0.00 	17 - 0.81		0 - 0.00		3 - 1.00		0 - 0.00	4 - 1.00	3 - 1.00	0 - 0.00		22 - 0.88	14 - 1.00	11 - 0.65			4 - 1.00	0 - 0.00		0 - 0.00	0 - 0.00 		19 - 1.00		6 - 0.75	1 -1.00			0 - 0.00	0 - 0.00	11 - 1.00	14 - 1.00		14 - 1.00	5 - 0.45							34 - 1.00	7 - 1.00	2 - 1.00	Nathan Copeland
"Mammary patterning phenotypes of A/J, C57BL/6, and 30 AXB/BXA recombinant inbred strains"	Number of super-numerary nipple or MG	Mammary gland patterning in the AXB/BXA recombinant inbred strains of mouse.		Mech Dev	2000	Mar	"Howard BA, Gusterson BA"	10704854		female	Feb-75		13 - 0.31		0 - 0.00		1 - 0.11	3 - 0.30		3 - 0.33	0 - 0.00	6 - 0.29		0 - 0.00		0 - 0.00		0 - 0.00	0 - 0.00	0 - 0.00	0 - 0.00		1 - 0.04 	1 - 0.07	0 - 0.00			0 - 0.00	0 - 0.00		0 - 0.00	0 - 0.00		6 - 0.32		2 - 0.25	0- 0.00			0 - 0.00	0 - 0.00	2 - 0.18	10 - 0.59		7 - 0.50	0 - 0.00							10 - 0.29	1 - 0.14	1 - 0.50	Nathan Copeland
"Mammary patterning phenotypes of A/J, C57BL/6, and 30 AXB/BXA recombinant inbred strains"	Number of misplaced MG - percent of total	Mammary gland patterning in the AXB/BXA recombinant inbred strains of mouse.		Mech Dev	2000	Mar	"Howard BA, Gusterson BA"	10704854		female	Feb-75		12 - 0.29		0 - 0.00		7 - 0.78	10 - 1.00		9 - 1.00	0 - 0.00	15 - 0.71		0 - 0.00		1 - 0.33		0 - 0.00	4 - 1.00	3 - 1.00	0 - 0.00		20 - 0.80	14 - 1.00	13 - 0.76			3 - 0.75	0 - 0.00		0 - 0.00	0 - 0.00		15 - 0.79		6 - 0.75	1 - 1.00			0- 0.00	0 - 0.00	8 - 0.73	14 - 0.82		13 - 0.93	5 - 0.45							29 - 0.85	7 - 1.00	1 - 0.50	Nathan Copeland
"Mammary patterning phenotypes of A/J, C57BL/6, and 30 AXB/BXA recombinant inbred strains"	Number of absent #3 MG - percent of total	Mammary gland patterning in the AXB/BXA recombinant inbred strains of mouse.		Mech Dev	2000	Mar	"Howard BA, Gusterson BA"	10704854		female	Feb-75		23 - 0.55		0 - 0.00		0 - 0.00	0 - 0.00		0 - 0.00	0 - 0.00	0 - 0.00		0 - 0.00		2 - 0.67		0 - 0.00	0 - 0.00	0 - 0.00	0 - 0.00	 	1 - 0.04	0 - 0.00	0 - 0.00			1 - 0.25	0- 0.00		0 - 0.00	0 - 0.00		2 - 0.11		0 - 0.00	0 - 0.00			0 - 0.00	0 - 0.00	3 - 0.27	2 - 0.12		0 - 0.00	0 - 0.00							0 - 0.00	0 - 0.00	0 - 0.00	Nathan Copeland
"Mammary patterning phenotypes of A/J, C57BL/6, and 30 AXB/BXA recombinant inbred strains"	Number of normal MG pattern phenotype -  percent of total	Mammary gland patterning in the AXB/BXA recombinant inbred strains of mouse.		Mech Dev	2000	Mar	"Howard BA, Gusterson BA"	10704854		female	Feb-75		2 - 0.05		75 - 1.00		1 - 0.11	0 - 0.00		0 - 0.00	5 - 1.00	4 - 0.19		24 - 1.00		0 - 0.00		6 - 1.00	0 - 0.00	0 - 0.00	13 - 1.00		3 - 0.12	0 - 0.00	6 - 0.35			0 - 0.00	10 - 1.00		32 - 1.00	14 - 1.00		0 - 0.00		2 - 0.25	0 - 0.00			29 - 1.00	4 - 1.00	0 - 0.00	0 - 0.00		0 - 0.00	6 - 0.55							4 - 0.12	0  - 0.00	0 - 0.00	Nathan Copeland
Strain distribution pattern of ska mammary gland phenotype of 30 AXXB/BXA recombinant inbred strains and localization of ska candidate locus on Chr 14	Dl4Mit207	Mammary gland patterning in the AXB/BXA recombinant inbred strains of mouse.		Mech Dev	2000	Mar	"Howard BA, Gusterson BA"	10704854		female	Feb-75	"A = (A/J) the ska mutation or A allele having  abnormal mammary gland pattern (misplaced nipples, absent glands, supernumerary nipples)B = (B6) The ska mutation or allele displaying normal mammary gland pattern (ten nipples and glands bilaterally symmetric)"					A	A		A	B	A		B		B		B	B	B	B		B	B	B			B	B		B	B		B		B	B			B	B	A	B		A	B							B	A	B	Nathan Copeland
Strain distribution pattern of ska mammary gland phenotype of 30 AXXB/BXA recombinant inbred strains and localization of ska candidate locus on Chr 14	Dl4Mit201	Mammary gland patterning in the AXB/BXA recombinant inbred strains of mouse.		Mech Dev	2000	Mar	"Howard BA, Gusterson BA"	10704854		female	Feb-75	"A = (A/J) the ska mutation or A allele having  abnormal mammary gland pattern (misplaced nipples, absent glands, supernumerary nipples)B = (B6) The ska mutation or allele displaying normal mammary gland pattern (ten nipples and glands bilaterally symmetric)"					A	A		A	B	A		B		A		B	B	A	B		B	B	B			B	B		B	B		B		B	A			B	B	A	B		A	A							B	A	B	Nathan Copeland
Strain distribution pattern of ska mammary gland phenotype of 30 AXXB/BXA recombinant inbred strains and localization of ska candidate locus on Chr 14	Dl4Mit202	Mammary gland patterning in the AXB/BXA recombinant inbred strains of mouse.		Mech Dev	2000	Mar	"Howard BA, Gusterson BA"	10704854		female	Feb-75	"A = (A/J) the ska mutation or A allele having  abnormal mammary gland pattern (misplaced nipples, absent glands, supernumerary nipples)B = (B6) The ska mutation or allele displaying normal mammary gland pattern (ten nipples and glands bilaterally symmetric)"					A	A		A	B	A		B		A		B	B	B	B		B	B	B			B	B		B	B		B		B	A			B	B	A	B		A	A							B	A	B	Nathan Copeland
Strain distribution pattern of ska mammary gland phenotype of 30 AXXB/BXA recombinant inbred strains and localization of ska candidate locus on Chr 14	Dl4Mit14	Mammary gland patterning in the AXB/BXA recombinant inbred strains of mouse.		Mech Dev	2000	Mar	"Howard BA, Gusterson BA"	10704854		female	Feb-75	"A = (A/J) the ska mutation or A allele having  abnormal mammary gland pattern (misplaced nipples, absent glands, supernumerary nipples)B = (B6) The ska mutation or allele displaying normal mammary gland pattern (ten nipples and glands bilaterally symmetric)"					A	A		A	B	A		B		A		B	B	B	B		B	B	B			A	B		B	B		B		B	A			B	B	A	B		A	A							B	A	B	Nathan Copeland
Strain distribution pattern of ska mammary gland phenotype of 30 AXXB/BXA recombinant inbred strains and localization of ska candidate locus on Chr 14	ska	Mammary gland patterning in the AXB/BXA recombinant inbred strains of mouse.		Mech Dev	2000	Mar	"Howard BA, Gusterson BA"	10704854		female	Feb-75	"A = (A/J) the ska mutation or A allele having  abnormal mammary gland pattern (misplaced nipples, absent glands, supernumerary nipples)B = (B6) The ska mutation or allele displaying normal mammary gland pattern (ten nipples and glands bilaterally symmetric)"					A	A		A	B	A		B		A		B	A	A	B		A	A	A			A	B		B	B		A		A	A			B	B	A	A		A	A							A	A	A	Nathan Copeland
Strain distribution pattern of ska mammary gland phenotype of 30 AXXB/BXA recombinant inbred strains and localization of ska candidate locus on Chr 14	Dl4Mit80	Mammary gland patterning in the AXB/BXA recombinant inbred strains of mouse.		Mech Dev	2000	Mar	"Howard BA, Gusterson BA"	10704854		female	Feb-75	"A = (A/J) the ska mutation or A allele having  abnormal mammary gland pattern (misplaced nipples, absent glands, supernumerary nipples)B = (B6) The ska mutation or allele displaying normal mammary gland pattern (ten nipples and glands bilaterally symmetric)"					B	A		A	B	A		B		B		B	B	A	B		B	B	B			A	B		B	B		B		A	A			B	B	A	A		A	A							A	A	A	Nathan Copeland
Strain distribution pattern of ska mammary gland phenotype of 30 AXXB/BXA recombinant inbred strains and localization of ska candidate locus on Chr 14	Dl4Mit29	Mammary gland patterning in the AXB/BXA recombinant inbred strains of mouse.		Mech Dev	2000	Mar	"Howard BA, Gusterson BA"	10704854		female	Feb-75	"A = (A/J) the ska mutation or A allele having  abnormal mammary gland pattern (misplaced nipples, absent glands, supernumerary nipples)B = (B6) The ska mutation or allele displaying normal mammary gland pattern (ten nipples and glands bilaterally symmetric)"					B	A		A	B	A		B		B		B	B	B	B		B	B	B			A	B		B	B		B		A	A			B	B	A	A		A	A							A	A	A	Nathan Copeland
The effect of MHV- 3 infection on inbred and Ri strains	H - 2 haplotype 	Susceptibility/resistance to mouse hepatitis virus strain 3 and macrophage procoagulant activity are genetically linked and controlled by two non-H-2-linked genes.	"The mode of inheritance of susceptibility/resistance to mouse hepatitis strain 3 (MHV-3) was determined by typing the set of AXB/BXA recombinant inbred (RI) strains derived from resistant A/J (A) and susceptible C57BL/6J (B) progenitors for susceptibility to infection as determined by the severity of liver pathology. The strain distribution pattern for susceptibility showed a discontinuous variation: one strain was fully resistant (A-like), four strains were fully susceptible (B-like), and 16 strains showed an intermediate degree of susceptibility. The fully susceptible strains developed fulminant hepatitis and died; the fully resistant strain developed no liver disease, whereas a range of disease ranging from mild focal hepatitis to widespread hepatocellular necrosis was seen in the semisusceptible strains. This SDP best fits the two-recessive-gene model of inheritance, and neither of these two loci is linked to the H-2 complex. Macrophage procoagulant activity (PCA) segregated among the RI strains in a strain distribution pattern identical to that of susceptibility/resistance. PCA levels were greater than sevenfold elevated in fully susceptible RI mice and fourfold elevated in semisusceptible mice with no increase in resistant mice. These observations suggest genetic linkage of susceptibility/resistance to MHV-3 infection and macrophage PCA."	J Immunol	1986	Oct	"Dindzans VJ, Skamene E, Levy GA."	3020124	6 - 8 weeks	both			a		b		a	a	a	a	a	b	a	a	a	b		a				a	b								b	b					a		b		a	b	b													Nathan Copeland
The effect of MHV- 3 infection on inbred and Ri strains	susceptibility 	Susceptibility/resistance to mouse hepatitis virus strain 3 and macrophage procoagulant activity are genetically linked and controlled by two non-H-2-linked genes.	"The mode of inheritance of susceptibility/resistance to mouse hepatitis strain 3 (MHV-3) was determined by typing the set of AXB/BXA recombinant inbred (RI) strains derived from resistant A/J (A) and susceptible C57BL/6J (B) progenitors for susceptibility to infection as determined by the severity of liver pathology. The strain distribution pattern for susceptibility showed a discontinuous variation: one strain was fully resistant (A-like), four strains were fully susceptible (B-like), and 16 strains showed an intermediate degree of susceptibility. The fully susceptible strains developed fulminant hepatitis and died; the fully resistant strain developed no liver disease, whereas a range of disease ranging from mild focal hepatitis to widespread hepatocellular necrosis was seen in the semisusceptible strains. This SDP best fits the two-recessive-gene model of inheritance, and neither of these two loci is linked to the H-2 complex. Macrophage procoagulant activity (PCA) segregated among the RI strains in a strain distribution pattern identical to that of susceptibility/resistance. PCA levels were greater than sevenfold elevated in fully susceptible RI mice and fourfold elevated in semisusceptible mice with no increase in resistant mice. These observations suggest genetic linkage of susceptibility/resistance to MHV-3 infection and macrophage PCA."	J Immunol	1986	Oct	"Dindzans VJ, Skamene E, Levy GA."	3020124	6 - 8 weeks	both		S = susceptible; R = resistant; SS = semisusceptible	R		S		SS	SS	S	SS	R	SS	SS	S	SS	S		SS				SS	SS								SS	SS					SS		SS		S	SS	SS													Nathan Copeland
The effect of MHV- 3 infection on inbred and Ri strains	mortality	Susceptibility/resistance to mouse hepatitis virus strain 3 and macrophage procoagulant activity are genetically linked and controlled by two non-H-2-linked genes.	"The mode of inheritance of susceptibility/resistance to mouse hepatitis strain 3 (MHV-3) was determined by typing the set of AXB/BXA recombinant inbred (RI) strains derived from resistant A/J (A) and susceptible C57BL/6J (B) progenitors for susceptibility to infection as determined by the severity of liver pathology. The strain distribution pattern for susceptibility showed a discontinuous variation: one strain was fully resistant (A-like), four strains were fully susceptible (B-like), and 16 strains showed an intermediate degree of susceptibility. The fully susceptible strains developed fulminant hepatitis and died; the fully resistant strain developed no liver disease, whereas a range of disease ranging from mild focal hepatitis to widespread hepatocellular necrosis was seen in the semisusceptible strains. This SDP best fits the two-recessive-gene model of inheritance, and neither of these two loci is linked to the H-2 complex. Macrophage procoagulant activity (PCA) segregated among the RI strains in a strain distribution pattern identical to that of susceptibility/resistance. PCA levels were greater than sevenfold elevated in fully susceptible RI mice and fourfold elevated in semisusceptible mice with no increase in resistant mice. These observations suggest genetic linkage of susceptibility/resistance to MHV-3 infection and macrophage PCA."	J Immunol	1986	Oct	"Dindzans VJ, Skamene E, Levy GA."	3020124	6 - 8 weeks	both		%	0		100		90	0	100	50	0	50	0	100	0	100		0				0	0								0	100					0		0		100	0	0													Nathan Copeland
The effect of MHV- 3 infection on inbred and Ri strains	PCA	Susceptibility/resistance to mouse hepatitis virus strain 3 and macrophage procoagulant activity are genetically linked and controlled by two non-H-2-linked genes.	"The mode of inheritance of susceptibility/resistance to mouse hepatitis strain 3 (MHV-3) was determined by typing the set of AXB/BXA recombinant inbred (RI) strains derived from resistant A/J (A) and susceptible C57BL/6J (B) progenitors for susceptibility to infection as determined by the severity of liver pathology. The strain distribution pattern for susceptibility showed a discontinuous variation: one strain was fully resistant (A-like), four strains were fully susceptible (B-like), and 16 strains showed an intermediate degree of susceptibility. The fully susceptible strains developed fulminant hepatitis and died; the fully resistant strain developed no liver disease, whereas a range of disease ranging from mild focal hepatitis to widespread hepatocellular necrosis was seen in the semisusceptible strains. This SDP best fits the two-recessive-gene model of inheritance, and neither of these two loci is linked to the H-2 complex. Macrophage procoagulant activity (PCA) segregated among the RI strains in a strain distribution pattern identical to that of susceptibility/resistance. PCA levels were greater than sevenfold elevated in fully susceptible RI mice and fourfold elevated in semisusceptible mice with no increase in resistant mice. These observations suggest genetic linkage of susceptibility/resistance to MHV-3 infection and macrophage PCA."	J Immunol	1986	Oct	"Dindzans VJ, Skamene E, Levy GA."	3020124	6 - 8 weeks	both		mU/ 10 ^6 SM (PCA of control mice = 253 +/- 190 mU/ 10^6 SM)	290		2400		100	1150	1770	1350	270	770	650	1770	1150	1900		1000				723	1300								1200	740					1000		770		1700	1000	850													Nathan Copeland
The effect of MHV- 3 infection on inbred and Ri strains	ALT	Susceptibility/resistance to mouse hepatitis virus strain 3 and macrophage procoagulant activity are genetically linked and controlled by two non-H-2-linked genes.	"The mode of inheritance of susceptibility/resistance to mouse hepatitis strain 3 (MHV-3) was determined by typing the set of AXB/BXA recombinant inbred (RI) strains derived from resistant A/J (A) and susceptible C57BL/6J (B) progenitors for susceptibility to infection as determined by the severity of liver pathology. The strain distribution pattern for susceptibility showed a discontinuous variation: one strain was fully resistant (A-like), four strains were fully susceptible (B-like), and 16 strains showed an intermediate degree of susceptibility. The fully susceptible strains developed fulminant hepatitis and died; the fully resistant strain developed no liver disease, whereas a range of disease ranging from mild focal hepatitis to widespread hepatocellular necrosis was seen in the semisusceptible strains. This SDP best fits the two-recessive-gene model of inheritance, and neither of these two loci is linked to the H-2 complex. Macrophage procoagulant activity (PCA) segregated among the RI strains in a strain distribution pattern identical to that of susceptibility/resistance. PCA levels were greater than sevenfold elevated in fully susceptible RI mice and fourfold elevated in semisusceptible mice with no increase in resistant mice. These observations suggest genetic linkage of susceptibility/resistance to MHV-3 infection and macrophage PCA."	J Immunol	1986	Oct	"Dindzans VJ, Skamene E, Levy GA."	3020124	6 - 8 weeks	both		IU/ L	15		1200		450	27	1000	360	15	61	24	850	41	700		41				25	46								15	194					10		24		308	8	0													Nathan Copeland
The effect of MHV- 3 infection on inbred and Ri strains	Viral titers	Susceptibility/resistance to mouse hepatitis virus strain 3 and macrophage procoagulant activity are genetically linked and controlled by two non-H-2-linked genes.	"The mode of inheritance of susceptibility/resistance to mouse hepatitis strain 3 (MHV-3) was determined by typing the set of AXB/BXA recombinant inbred (RI) strains derived from resistant A/J (A) and susceptible C57BL/6J (B) progenitors for susceptibility to infection as determined by the severity of liver pathology. The strain distribution pattern for susceptibility showed a discontinuous variation: one strain was fully resistant (A-like), four strains were fully susceptible (B-like), and 16 strains showed an intermediate degree of susceptibility. The fully susceptible strains developed fulminant hepatitis and died; the fully resistant strain developed no liver disease, whereas a range of disease ranging from mild focal hepatitis to widespread hepatocellular necrosis was seen in the semisusceptible strains. This SDP best fits the two-recessive-gene model of inheritance, and neither of these two loci is linked to the H-2 complex. Macrophage procoagulant activity (PCA) segregated among the RI strains in a strain distribution pattern identical to that of susceptibility/resistance. PCA levels were greater than sevenfold elevated in fully susceptible RI mice and fourfold elevated in semisusceptible mice with no increase in resistant mice. These observations suggest genetic linkage of susceptibility/resistance to MHV-3 infection and macrophage PCA."	J Immunol	1986	Oct	"Dindzans VJ, Skamene E, Levy GA."	3020124	6 - 8 weeks	both		PFU/ g liver	1 x 10^4		4 x 10^7		3.2 x 10^7	4.5 x 10^3	3.3 x 10^6	8.0 x 10^5	1.2 x 10^5	4.5 x 10^3	1.1 x 10^4	5.0 x 10^6	4.0 x 10^6	1.5 x 10^5		2.3 x 10^5				8.5 x 10^3	7.0 x 10^4								1.9 x 10^4	1.1 x 10^7					2.0 x 10^4		7.5 x 10^3		2.0 x 10^4	7.5 x 10^3	5.0 x 10^6													Nathan Copeland
Pulmonary tumors in AXB and BXA RI mice	Mean number of tumors/ mouse	Susceptibility to urethan-induced pulmonary adenomas between A/J and C57BL/6J mice: use of AXB and BXA recombinant inbred lines indicating a three-locus genetic model.	"For insight into the number of genes governing differential susceptibility such as in mice of the inbred strain A/J (A) highly susceptible to the induction of pulmonary adenomas by urethan in comparison to resistant strain C57BL/6J (B6) mice, tumor induction was studied in the AXB and BXA series of recombinant inbred (RI) strains derived respectively from A female X B6 male and B6 female X A male ancestral lines. Mice from 46 of these lines were given injections with 1 mg urethan/g (body wt), and the tumor number was assessed 4 months later. Lung tumor multiplicity for several RI lines was independently characterized in the Boulder, CO, and Montreal laboratories, and very similar numbers were obtained. Most lines had multiplicities intermediate to those of the progenitor strains, clearly indicating that more than a single gene accounted for the differences in lung tumor susceptibility between A and B6. The tumor incidence and multiplicity data fit very closely to what would be expected under a three-locus model, and we designated these genes ""Pas"" for pulmonary adenoma susceptibility. One locus called ""Pas-1"" had an effect on tumor multiplicity greater than that of the other lo"	J Natl Cancer Inst	1985	Nov	"Malkinson AM, Nesbitt MN, Skamene E."	3863994	2 - 4 months	both	Feb-36		29.6		0.9		28.9	0.6	27.4	1.9	17.8	2.7	10	8.8	15.3	0.2	6.8	8.9	1.1	3.3	16.7	14	2	2	2	12.8	1	13.6	8	17.6	0.8	24.4	3.8	26.8	0.9	2	5.9	10.4	4.8	8.8	1.2	4.8	5.2		7.7	6.2	14.5	6.5	16		7.2	31	16	7.3		Nathan Copeland
Pulmonary tumors in AXB and BXA RI mice	SE	Susceptibility to urethan-induced pulmonary adenomas between A/J and C57BL/6J mice: use of AXB and BXA recombinant inbred lines indicating a three-locus genetic model.	"For insight into the number of genes governing differential susceptibility such as in mice of the inbred strain A/J (A) highly susceptible to the induction of pulmonary adenomas by urethan in comparison to resistant strain C57BL/6J (B6) mice, tumor induction was studied in the AXB and BXA series of recombinant inbred (RI) strains derived respectively from A female X B6 male and B6 female X A male ancestral lines. Mice from 46 of these lines were given injections with 1 mg urethan/g (body wt), and the tumor number was assessed 4 months later. Lung tumor multiplicity for several RI lines was independently characterized in the Boulder, CO, and Montreal laboratories, and very similar numbers were obtained. Most lines had multiplicities intermediate to those of the progenitor strains, clearly indicating that more than a single gene accounted for the differences in lung tumor susceptibility between A and B6. The tumor incidence and multiplicity data fit very closely to what would be expected under a three-locus model, and we designated these genes ""Pas"" for pulmonary adenoma susceptibility. One locus called ""Pas-1"" had an effect on tumor multiplicity greater than that of the other lo"	J Natl Cancer Inst	1985	Nov	"Malkinson AM, Nesbitt MN, Skamene E."	3863994	2 - 4 months	both	Feb-36		1.65		0.21		2.05	0.23	3.83	0.76	2.42	0.37	0.71	2.6	1.25	0.17	1.14	1.05	0.55	0.99	2.45	1.29	0.84	0.68	0.41	1.53		2.32	0.86	3.53	0.31	1.78	0.37	4.98	0.23	0.41	0.64	1.99	2.52	1.35	0.6	0.63	1.01		2.06	1.72	1.88	0.56	2.42		1.11	4.73	2.02	2.23		Nathan Copeland
Pulmonary tumors in AXB and BXA RI mice	Fraction of mice with no tumors - number of mice with no tumors/ total number of mice	Susceptibility to urethan-induced pulmonary adenomas between A/J and C57BL/6J mice: use of AXB and BXA recombinant inbred lines indicating a three-locus genetic model.	"For insight into the number of genes governing differential susceptibility such as in mice of the inbred strain A/J (A) highly susceptible to the induction of pulmonary adenomas by urethan in comparison to resistant strain C57BL/6J (B6) mice, tumor induction was studied in the AXB and BXA series of recombinant inbred (RI) strains derived respectively from A female X B6 male and B6 female X A male ancestral lines. Mice from 46 of these lines were given injections with 1 mg urethan/g (body wt), and the tumor number was assessed 4 months later. Lung tumor multiplicity for several RI lines was independently characterized in the Boulder, CO, and Montreal laboratories, and very similar numbers were obtained. Most lines had multiplicities intermediate to those of the progenitor strains, clearly indicating that more than a single gene accounted for the differences in lung tumor susceptibility between A and B6. The tumor incidence and multiplicity data fit very closely to what would be expected under a three-locus model, and we designated these genes ""Pas"" for pulmonary adenoma susceptibility. One locus called ""Pas-1"" had an effect on tumor multiplicity greater than that of the other lo"	J Natl Cancer Inst	1985	Nov	"Malkinson AM, Nesbitt MN, Skamene E."	3863994	2 - 4 months	both	Feb-36		None		0.52 - 16/31		None	0.64 - 9/14	None	0.27 - 3/11	None	0.14 - 3/22	None	None	None	0.83 - 5/6	None	None	0.57 - 4/7	0.17 - 1/6	None	None	0.20 - 1/5	0.17 - 1/6	None	None	None	None	None	None	0.56 - 9/16	None	None	None	0.50 - 12/24	None	None	None	0.20 - 1/5	None	0.33 - 2/6	None	0.17 - 2/12		None	None	None	None	None		None	None	None	None		Nathan Copeland
Pulmonary tumors in AXB and BXA RI mice	putative genotype	Susceptibility to urethan-induced pulmonary adenomas between A/J and C57BL/6J mice: use of AXB and BXA recombinant inbred lines indicating a three-locus genetic model.	"For insight into the number of genes governing differential susceptibility such as in mice of the inbred strain A/J (A) highly susceptible to the induction of pulmonary adenomas by urethan in comparison to resistant strain C57BL/6J (B6) mice, tumor induction was studied in the AXB and BXA series of recombinant inbred (RI) strains derived respectively from A female X B6 male and B6 female X A male ancestral lines. Mice from 46 of these lines were given injections with 1 mg urethan/g (body wt), and the tumor number was assessed 4 months later. Lung tumor multiplicity for several RI lines was independently characterized in the Boulder, CO, and Montreal laboratories, and very similar numbers were obtained. Most lines had multiplicities intermediate to those of the progenitor strains, clearly indicating that more than a single gene accounted for the differences in lung tumor susceptibility between A and B6. The tumor incidence and multiplicity data fit very closely to what would be expected under a three-locus model, and we designated these genes ""Pas"" for pulmonary adenoma susceptibility. One locus called ""Pas-1"" had an effect on tumor multiplicity greater than that of the other lo"	J Natl Cancer Inst	1985	Nov	"Malkinson AM, Nesbitt MN, Skamene E."	3863994	2 - 4 months	both	Feb-36	the first letter refers to the allele at Pas -1	AAA		BBB		AAA	BBB	AAA	B(B-)	A(B-)	B(A-)	B(A-)	B(A-)	A(B-)	BBB	B(B-)	B(A-)	BBB	B(B-)	A(B-)	A(B-)	B(B-)	B(B-)	B(B-)	A(B-)	BBB	A(B-)	B(A-)	A(B-)	BBB	A(A-)	B(B-)	AAA	BBB	B(B-)	B(A-)	B(A-)	B(A-)	B(A-)	BBB	B(A-)	B(A-)		B(A-)	B(A-)	A(B-)	B(A-)	A(B-)		B(A-)	AAA	A(B-)	B(A-)		Nathan Copeland
KRAS2 genotype and tumor susceptibility in idividual Ri strains	KRAS2 gentoype	KRAS2 as a genetic marker for lung tumor susceptibility in inbred mice.	"An Eco-RI restriction fragment length polymorphism occurring in a DNA fragment containing the first exon of the murine KRAS2 gene was shown to correlate with the inherited susceptibility of inbred strains of mice to urethan (CAS: 51-79-6)-induced pulmonary adenomas. Eco-RI digestion of murine DNA yielded four KRAS2-specific fragments. Polymorphic variation occurred in the smallest molecular-weight fragment with alleles of either 0.70 or 0.55 kb in size. Genotyping of 14 inbred strains of mice revealed a correlation between KRAS2 Eco-RI polymorphic variation and the differential susceptibility among inbred strains to development of pulmonary adenomas. Strains with a high incidence of pulmonary adenomas, either spontaneously occurring or in response to carcinogen induction, had the 0.55-kb KRAS2 allele whereas adenoma-resistant strains had the 0.70-kb allele. Analysis of a series of recombinant inbred strains (AXB, BXA) that developed from reciprocal crosses between a highly susceptible strain (A/J) and a highly resistant strain (C57BL/6J) revealed a statistically significant threefold difference in lung tumor susceptibility on the basis of KRAS2 genotype. Further analysis of individual F2 mice of a C57BL/6 female X A/J male cross also demonstrated a threefold difference in tumor susceptibility on the basis of KRAS2 allelic variation."	: J Natl Cancer Inst 	1987	Dec	"Ryan J, Barker PE, Nesbitt MN, Ruddle FH."	2891865	5 weeks	both							0.55	0.7	0.55	0.77	0.55	0.55	0.7	0.55	0.7	0.7	0.7	0.55	0.7	0.7	0.55	0.55		0.7	0.7	0.55	0.7	0.55	0.7		0.7	0.7		0.55	heterozygous		heterozygous	0.55	0.55		0.7	0.7	0.55		0.55	heterozygous	0.7	0.7	0.55		0.55	0.55	0.55	0.7		Nathan Copeland
KRAS2 genotype and tumor susceptibility in idividual Ri strains	Meanumber tumors/ mouse +/- SE	KRAS2 as a genetic marker for lung tumor susceptibility in inbred mice.	"An Eco-RI restriction fragment length polymorphism occurring in a DNA fragment containing the first exon of the murine KRAS2 gene was shown to correlate with the inherited susceptibility of inbred strains of mice to urethan (CAS: 51-79-6)-induced pulmonary adenomas. Eco-RI digestion of murine DNA yielded four KRAS2-specific fragments. Polymorphic variation occurred in the smallest molecular-weight fragment with alleles of either 0.70 or 0.55 kb in size. Genotyping of 14 inbred strains of mice revealed a correlation between KRAS2 Eco-RI polymorphic variation and the differential susceptibility among inbred strains to development of pulmonary adenomas. Strains with a high incidence of pulmonary adenomas, either spontaneously occurring or in response to carcinogen induction, had the 0.55-kb KRAS2 allele whereas adenoma-resistant strains had the 0.70-kb allele. Analysis of a series of recombinant inbred strains (AXB, BXA) that developed from reciprocal crosses between a highly susceptible strain (A/J) and a highly resistant strain (C57BL/6J) revealed a statistically significant threefold difference in lung tumor susceptibility on the basis of KRAS2 genotype. Further analysis of individual F2 mice of a C57BL/6 female X A/J male cross also demonstrated a threefold difference in tumor susceptibility on the basis of KRAS2 allelic variation."	: J Natl Cancer Inst 	1987	Dec	"Ryan J, Barker PE, Nesbitt MN, Ruddle FH."	2891865	5 weeks	both							28.9 +/- 2.05	0.6 +/- 0.23	27.4 +/- 3.83	1.9 +/- 0.76	17.8 +/-  2.42	2.7  +/- 0.37	10.0 +/- 0.71	8.8 +/- 2.60 	15.3 +/- 1.25	0.2 +/-  0.71	6.8 +/- 1.14	8.9 +/- 1.05	1.1 +/- 0.55	3.3 +/- 0.99	16.7 +/- 2.45	14.0 +/- 1.29		2.0 +/- 0.68	2.0 +/- 0.41	12.8 +/- 1.53	1.1 +/- 0.63	13.6 +/- 2.32	8.0 +/- 0.86		0.8 +/- 0.31	24.4 +/- 1.78		26.8 +/- 4.98	5.9 +/- 0.64		5.9 +/- 0.64	10.4 +/- 1.99	4.8 +/- 2.52		1.2 +/- 0.60	4.8 +/- 0.63	5.2 +/- 1.01		7.7 +/- 2.06	6.2 +/- 1.72	14.5 +/- 1.88	6.5 +/- 0.56	16.0 +/- 2.42		7.2 +/- 1.11	31.0 +/- 4.73	16.0 +/- 2.02	7.3 +/- 2.23		Nathan Copeland
Co- segregating of the traits of resistance/ siscetobo;otu tp BCG and In Vitro Macrophange Killing of M. Smergmatis	log CFU/ spleen	Killing of Mycobacterium smegmatis by macrophages from genetically susceptible and resistant mice.	"The bactericidal function of macrophages was investigated in congenic mice expressing the phenotype of susceptibility (B10.A, Bcgs) or resistance (B10.ABcgr) to mycobacterial infection. When splenic and peritoneal macrophages from these two mouse strains were infected in vitro with Mycobacterium smegmatis, the Bcgr macrophages were shown to inactivate M. smegmatis more efficiently than their Bcgs congenic counterparts. The mechanisms of this superior antimycobacterial activity was studied further. Addition of catalase did not abolish killing to a significant degree in either allelic type of macrophage, suggesting that hydrogen peroxide production was not involved in the killing activity controlled by the Bcg gene. Activation of Bcgs macrophages by exposure to crude lymphokines rendered them equally as efficient as their Bcgr counterparts in their capacity to destroy M. smegmatis. This finding suggests that both the genetically resistant and susceptible macrophages have the potential to kill M. smegmatis in vitro. This potential is expressed constitutively by the Bcgr but not Bcgs macrophages and can be induced, by lymphokine treatment, in the Bcgs macrophages. In a final set of experiments, the macrophage killing of M. smegmatis was evaluated as a test system to type for the Bcg gene allelic type in vitro, using a set of AXB and BXA recombinant inbred strains of mice. Results obtained show that typing of AXB/BXA recombinant inbred strains for the trait of bactericidal activity vs. M. smegmatis in vitro revealed a perfect match with the strain distribution pattern of resistance/susceptibility to Mycobacterium "	J Leukoc Biol	1990	Jan	"Denis M, Forget A, Pelletier M, Gervais F, Skamene E."	2294152		both			4.1	B10.A (Bcgs) = 5.2	B10.A(Bcgr) = 3.8		5.8	3.9				5.1	4									3.7													5.5		4.2																			Nathan Copeland
Co- segregating of the traits of resistance/ siscetobo;otu tp BCG and In Vitro Macrophange Killing of M. Smergmatis	Bcg allelic type	Killing of Mycobacterium smegmatis by macrophages from genetically susceptible and resistant mice.	"The bactericidal function of macrophages was investigated in congenic mice expressing the phenotype of susceptibility (B10.A, Bcgs) or resistance (B10.ABcgr) to mycobacterial infection. When splenic and peritoneal macrophages from these two mouse strains were infected in vitro with Mycobacterium smegmatis, the Bcgr macrophages were shown to inactivate M. smegmatis more efficiently than their Bcgs congenic counterparts. The mechanisms of this superior antimycobacterial activity was studied further. Addition of catalase did not abolish killing to a significant degree in either allelic type of macrophage, suggesting that hydrogen peroxide production was not involved in the killing activity controlled by the Bcg gene. Activation of Bcgs macrophages by exposure to crude lymphokines rendered them equally as efficient as their Bcgr counterparts in their capacity to destroy M. smegmatis. This finding suggests that both the genetically resistant and susceptible macrophages have the potential to kill M. smegmatis in vitro. This potential is expressed constitutively by the Bcgr but not Bcgs macrophages and can be induced, by lymphokine treatment, in the Bcgs macrophages. In a final set of experiments, the macrophage killing of M. smegmatis was evaluated as a test system to type for the Bcg gene allelic type in vitro, using a set of AXB and BXA recombinant inbred strains of mice. Results obtained show that typing of AXB/BXA recombinant inbred strains for the trait of bactericidal activity vs. M. smegmatis in vitro revealed a perfect match with the strain distribution pattern of resistance/susceptibility to Mycobacterium "	J Leukoc Biol	1990	Jan	"Denis M, Forget A, Pelletier M, Gervais F, Skamene E."	2294152		both			s	B10.A (Bcgs) = s	B10.A(Bcgr) = r		r	r				s	r									r													s		r																			Nathan Copeland
Co- segregating of the traits of resistance/ siscetobo;otu tp BCG and In Vitro Macrophange Killing of M. Smergmatis	% killing of M. smegmatis in vitro	Killing of Mycobacterium smegmatis by macrophages from genetically susceptible and resistant mice.	"The bactericidal function of macrophages was investigated in congenic mice expressing the phenotype of susceptibility (B10.A, Bcgs) or resistance (B10.ABcgr) to mycobacterial infection. When splenic and peritoneal macrophages from these two mouse strains were infected in vitro with Mycobacterium smegmatis, the Bcgr macrophages were shown to inactivate M. smegmatis more efficiently than their Bcgs congenic counterparts. The mechanisms of this superior antimycobacterial activity was studied further. Addition of catalase did not abolish killing to a significant degree in either allelic type of macrophage, suggesting that hydrogen peroxide production was not involved in the killing activity controlled by the Bcg gene. Activation of Bcgs macrophages by exposure to crude lymphokines rendered them equally as efficient as their Bcgr counterparts in their capacity to destroy M. smegmatis. This finding suggests that both the genetically resistant and susceptible macrophages have the potential to kill M. smegmatis in vitro. This potential is expressed constitutively by the Bcgr but not Bcgs macrophages and can be induced, by lymphokine treatment, in the Bcgs macrophages. In a final set of experiments, the macrophage killing of M. smegmatis was evaluated as a test system to type for the Bcg gene allelic type in vitro, using a set of AXB and BXA recombinant inbred strains of mice. Results obtained show that typing of AXB/BXA recombinant inbred strains for the trait of bactericidal activity vs. M. smegmatis in vitro revealed a perfect match with the strain distribution pattern of resistance/susceptibility to Mycobacterium "	J Leukoc Biol	1990	Jan	"Denis M, Forget A, Pelletier M, Gervais F, Skamene E."	2294152		both			3	B10.A (Bcgs) = 3	B10.A(Bcgr) = 52 		52	31				11	0									37													9		57																			Nathan Copeland
"Mean canonical variate values for A/J, C57BL/10J, two congenic strains and 19 recombinant inbred strains"	CV1	Genetic variation in the shape of the mouse mandible and its relationship to glucocorticoid-induced cleft palate analyzed by using recombinant inbred lines.	"Variation in mandible shape has been investigated in a set of recombinant inbred (RI) lines of mice, the C57BL/6J X A/J (BXA;AXB) RI lines. Considerable genetic variation was detected between the RI lines, but most lines were intermediate in shape when compared with the parent lines. Variation in mandible shape could not be explained by any single gene differences known between the parent lines including the H-2 locus. Some RI lines had mandible shapes unlike either parent, and one in particular, line BXA1, had an unusual shape with a pronounced condyloid process. It was concluded that mandible shape has a complex inheritance involving a number of genes, each with small effects. In some cases, recombination of the genes can produce bone shapes quite different from those of the original parent line.--There was no evidence that the variability in steroid-induced cleft palate incidence in the BXA;AXB RI lines is related to the variation in adult mandible shape as detected in this study."	Genetics	1986	July	"Lovell DP, Erickson RP."	3732791		both	5-Mar		-0.22	0.8	3.3	3.48	0.35	3.53			1.94; 0.65 	5.34	0.38 +/- 1.98		-1.76			2.02	1.26		-1.24	2.67									5.48	3.24		3.33	-1.16		1.52 ; 0.80 		-0.33	3.28 ; 4.27			0.85	-1.84 ; -1.02 												Nathan Copeland
"Mean canonical variate values for A/J, C57BL/10J, two congenic strains and 19 recombinant inbred strains"	CV2	Genetic variation in the shape of the mouse mandible and its relationship to glucocorticoid-induced cleft palate analyzed by using recombinant inbred lines.	"Variation in mandible shape has been investigated in a set of recombinant inbred (RI) lines of mice, the C57BL/6J X A/J (BXA;AXB) RI lines. Considerable genetic variation was detected between the RI lines, but most lines were intermediate in shape when compared with the parent lines. Variation in mandible shape could not be explained by any single gene differences known between the parent lines including the H-2 locus. Some RI lines had mandible shapes unlike either parent, and one in particular, line BXA1, had an unusual shape with a pronounced condyloid process. It was concluded that mandible shape has a complex inheritance involving a number of genes, each with small effects. In some cases, recombination of the genes can produce bone shapes quite different from those of the original parent line.--There was no evidence that the variability in steroid-induced cleft palate incidence in the BXA;AXB RI lines is related to the variation in adult mandible shape as detected in this study."	Genetics	1986	July	"Lovell DP, Erickson RP."	3732791		both	5-Mar		1.23	-0.32	-2.54	-3.49	-1.87	-2.4			-0.39 ; 0.27 	-2.05	-0.17 +/- 1.40		1.82			0.071	0.04		1.12	-0.41									-6.14	-3.56		1.46	-2.05		-0.74; -1.19 		2.17	-1.45;  -3.94 			0.21	2.82 ; -0.53												Nathan Copeland
"Mean canonical variate values for A/J, C57BL/10J, two congenic strains and 19 recombinant inbred strains"	CV3	Genetic variation in the shape of the mouse mandible and its relationship to glucocorticoid-induced cleft palate analyzed by using recombinant inbred lines.	"Variation in mandible shape has been investigated in a set of recombinant inbred (RI) lines of mice, the C57BL/6J X A/J (BXA;AXB) RI lines. Considerable genetic variation was detected between the RI lines, but most lines were intermediate in shape when compared with the parent lines. Variation in mandible shape could not be explained by any single gene differences known between the parent lines including the H-2 locus. Some RI lines had mandible shapes unlike either parent, and one in particular, line BXA1, had an unusual shape with a pronounced condyloid process. It was concluded that mandible shape has a complex inheritance involving a number of genes, each with small effects. In some cases, recombination of the genes can produce bone shapes quite different from those of the original parent line.--There was no evidence that the variability in steroid-induced cleft palate incidence in the BXA;AXB RI lines is related to the variation in adult mandible shape as detected in this study."	Genetics	1986	July	"Lovell DP, Erickson RP."	3732791		both	5-Mar		2.81	1.6	0.84	1.56	3.93	4.1			2.72 ;  2.45	3.76	2.77 +/- 0.48		-0.54			-1.03	4.8		1.86	3.08									5.2	2.5		3.07	5.46		4.66; 6.11 		5.07	0.79; 3.41 			3.08	2.40 ; 4.84 												Nathan Copeland
"Mean canonical variate values for A/J, C57BL/10J, two congenic strains and 19 recombinant inbred strains"	CV4	Genetic variation in the shape of the mouse mandible and its relationship to glucocorticoid-induced cleft palate analyzed by using recombinant inbred lines.	"Variation in mandible shape has been investigated in a set of recombinant inbred (RI) lines of mice, the C57BL/6J X A/J (BXA;AXB) RI lines. Considerable genetic variation was detected between the RI lines, but most lines were intermediate in shape when compared with the parent lines. Variation in mandible shape could not be explained by any single gene differences known between the parent lines including the H-2 locus. Some RI lines had mandible shapes unlike either parent, and one in particular, line BXA1, had an unusual shape with a pronounced condyloid process. It was concluded that mandible shape has a complex inheritance involving a number of genes, each with small effects. In some cases, recombination of the genes can produce bone shapes quite different from those of the original parent line.--There was no evidence that the variability in steroid-induced cleft palate incidence in the BXA;AXB RI lines is related to the variation in adult mandible shape as detected in this study."	Genetics	1986	July	"Lovell DP, Erickson RP."	3732791		both	5-Mar		1.44	-0.63	4.49	3.66	3.98	1.35			1.45 ; 1.74 	2.2	2.76 +/- 2.44		4.02			2.41	1.4		4.29	3.04									0.54	3.78		-1.17	1.88		1.52; -0.33 		-0.13	3.04; 5.28 			1.3	2.09 ; 4.51 												Nathan Copeland
"Mean canonical variate values for A/J, C57BL/10J, two congenic strains and 19 recombinant inbred strains"	% steroid - induced cleft palate	Genetic variation in the shape of the mouse mandible and its relationship to glucocorticoid-induced cleft palate analyzed by using recombinant inbred lines.	"Variation in mandible shape has been investigated in a set of recombinant inbred (RI) lines of mice, the C57BL/6J X A/J (BXA;AXB) RI lines. Considerable genetic variation was detected between the RI lines, but most lines were intermediate in shape when compared with the parent lines. Variation in mandible shape could not be explained by any single gene differences known between the parent lines including the H-2 locus. Some RI lines had mandible shapes unlike either parent, and one in particular, line BXA1, had an unusual shape with a pronounced condyloid process. It was concluded that mandible shape has a complex inheritance involving a number of genes, each with small effects. In some cases, recombination of the genes can produce bone shapes quite different from those of the original parent line.--There was no evidence that the variability in steroid-induced cleft palate incidence in the BXA;AXB RI lines is related to the variation in adult mandible shape as detected in this study."	Genetics	1986	July	"Lovell DP, Erickson RP."	3732791		both	5-Mar		24	22	1	8	9	6			12	1			24			13	8		0	0										1		21	6		0		0	0			35	5												Nathan Copeland
"Mean canonical variate values for A/J, C57BL/10J, two congenic strains and 19 recombinant inbred strains"	H-2	Genetic variation in the shape of the mouse mandible and its relationship to glucocorticoid-induced cleft palate analyzed by using recombinant inbred lines.	"Variation in mandible shape has been investigated in a set of recombinant inbred (RI) lines of mice, the C57BL/6J X A/J (BXA;AXB) RI lines. Considerable genetic variation was detected between the RI lines, but most lines were intermediate in shape when compared with the parent lines. Variation in mandible shape could not be explained by any single gene differences known between the parent lines including the H-2 locus. Some RI lines had mandible shapes unlike either parent, and one in particular, line BXA1, had an unusual shape with a pronounced condyloid process. It was concluded that mandible shape has a complex inheritance involving a number of genes, each with small effects. In some cases, recombination of the genes can produce bone shapes quite different from those of the original parent line.--There was no evidence that the variability in steroid-induced cleft palate incidence in the BXA;AXB RI lines is related to the variation in adult mandible shape as detected in this study."	Genetics	1986	July	"Lovell DP, Erickson RP."	3732791		both	5-Mar	A = A/J like; B = B57BL/6J	A	B	B	A	A	A			A	B	A		A			A	B		A	A									B	B		A	A		A		B	B			A	B												Nathan Copeland
"Mean canonical variate values for A/J, C57BL/10J, two congenic strains and 19 recombinant inbred strains"	 Beta 2m	Genetic variation in the shape of the mouse mandible and its relationship to glucocorticoid-induced cleft palate analyzed by using recombinant inbred lines.	"Variation in mandible shape has been investigated in a set of recombinant inbred (RI) lines of mice, the C57BL/6J X A/J (BXA;AXB) RI lines. Considerable genetic variation was detected between the RI lines, but most lines were intermediate in shape when compared with the parent lines. Variation in mandible shape could not be explained by any single gene differences known between the parent lines including the H-2 locus. Some RI lines had mandible shapes unlike either parent, and one in particular, line BXA1, had an unusual shape with a pronounced condyloid process. It was concluded that mandible shape has a complex inheritance involving a number of genes, each with small effects. In some cases, recombination of the genes can produce bone shapes quite different from those of the original parent line.--There was no evidence that the variability in steroid-induced cleft palate incidence in the BXA;AXB RI lines is related to the variation in adult mandible shape as detected in this study."	Genetics	1986	July	"Lovell DP, Erickson RP."	3732791		both	5-Mar	A = A/J like; B = B57BL/6J	A	A	B	B	A	B			A	A	B		A			A	B		A	A									A	A		B	A		B		A	B			B	A												Nathan Copeland
"Mean canonical variate values for A/J, C57BL/10J, two congenic strains and 19 recombinant inbred strains"	Gus	Genetic variation in the shape of the mouse mandible and its relationship to glucocorticoid-induced cleft palate analyzed by using recombinant inbred lines.	"Variation in mandible shape has been investigated in a set of recombinant inbred (RI) lines of mice, the C57BL/6J X A/J (BXA;AXB) RI lines. Considerable genetic variation was detected between the RI lines, but most lines were intermediate in shape when compared with the parent lines. Variation in mandible shape could not be explained by any single gene differences known between the parent lines including the H-2 locus. Some RI lines had mandible shapes unlike either parent, and one in particular, line BXA1, had an unusual shape with a pronounced condyloid process. It was concluded that mandible shape has a complex inheritance involving a number of genes, each with small effects. In some cases, recombination of the genes can produce bone shapes quite different from those of the original parent line.--There was no evidence that the variability in steroid-induced cleft palate incidence in the BXA;AXB RI lines is related to the variation in adult mandible shape as detected in this study."	Genetics	1986	July	"Lovell DP, Erickson RP."	3732791		both	5-Mar	A = A/J like; B = B57BL/6J	A	A	B	B	B	A			A	A	B		A			A	B			A									A	A		A	B				A	A			B	A												Nathan Copeland
Induction of anti-cardiac sarcolemmal antibody (ASA) in Coxsakievirus B3-infected AXB/BXA recombinant inbred strains	Prevalence 	Genetic control of Coxsackievirus B3-induced heart-specific autoantibodies associated with chronic myocarditis.	"Cardiac-specific autoantibodies to sarcolemmal and cardiac myosin antigens observed during the chronic phase of Coxsackievirus B3-induced myocarditis appear to be under autosomal recessive control. This observation is based on examination of F1 hybrids bred from A/J mice which develop chronic myocarditis and C57BL/6J mice which resolve the virus-induced lesions. Previous mouse studies demonstrated that the prevalence of heart-specific autoantibodies varied with the H-2 complex. However, in 25 H-2 congenic mouse strains the strain background was the predominant determinant of autoantibody presence. Recently, we extended our genetic evaluation of the chromosomal locations governing autoantibody responses by examining 25 AXB and BXA recombinant inbred strains. Two populations of heart-specific autoantibodies were demonstrated against sarcolemmal and cardiac myosin antigens. Analyses of the AXB/BXA strain distribution patterns for these two traits revealed that the anti-sarcolemmal response was controlled by a gene(s) linked to Np-2 and Ter alpha loci on chromosome 14. Linkage could not be assigned for the anti-cardiac myosin response."	Clin Exp Immunol	1991	Nov	"Traystman MD, Beisel KW."	1657464	2 weeks	both		Expressed as the number of positives over the  total numer examined. The percent prevalence is after the hyphen	33/91 - 36	35/160 - 22	0/118 - 0	0/95 - 0	1/11/09	10/21/48			0/ 29 - 0	7/11/64	0/18 - 0	1/11/09		0/10 - 0					9/19/47	5/30/17	4/22/18	0/21 - 0	0/19 - 0	0/14 - 0		4/9/44		3/26/12					5/10/50		3/10/30		0/16 - 0	0/17 - 0	1/17/06							3/19/16			8/11/73	5/8/63	3/17/18	4/24/17		Nathan Copeland
Induction of anti-cardiac sarcolemmal antibody (ASA) in Coxsakievirus B3-infected AXB/BXA recombinant inbred strains	Phenotype	Genetic control of Coxsackievirus B3-induced heart-specific autoantibodies associated with chronic myocarditis.	"Cardiac-specific autoantibodies to sarcolemmal and cardiac myosin antigens observed during the chronic phase of Coxsackievirus B3-induced myocarditis appear to be under autosomal recessive control. This observation is based on examination of F1 hybrids bred from A/J mice which develop chronic myocarditis and C57BL/6J mice which resolve the virus-induced lesions. Previous mouse studies demonstrated that the prevalence of heart-specific autoantibodies varied with the H-2 complex. However, in 25 H-2 congenic mouse strains the strain background was the predominant determinant of autoantibody presence. Recently, we extended our genetic evaluation of the chromosomal locations governing autoantibody responses by examining 25 AXB and BXA recombinant inbred strains. Two populations of heart-specific autoantibodies were demonstrated against sarcolemmal and cardiac myosin antigens. Analyses of the AXB/BXA strain distribution patterns for these two traits revealed that the anti-sarcolemmal response was controlled by a gene(s) linked to Np-2 and Ter alpha loci on chromosome 14. Linkage could not be assigned for the anti-cardiac myosin response."	Clin Exp Immunol	1991	Nov	"Traystman MD, Beisel KW."	1657464	2 weeks	both		A denotes the A/J parental trait and B denotes the trait of C57Bl/6J	A	A	B	B		A			B	A	B			B					A	B	B	B	B	B		A		B					A		A		B	B								A			A	A	A	A		Nathan Copeland
Production of cardiac myosin in Coxackie virus B3- infected AXB/BXA  mice	Cardiac myosin anutoantibody titre	Genetic control of Coxsackievirus B3-induced heart-specific autoantibodies associated with chronic myocarditis.	"Cardiac-specific autoantibodies to sarcolemmal and cardiac myosin antigens observed during the chronic phase of Coxsackievirus B3-induced myocarditis appear to be under autosomal recessive control. This observation is based on examination of F1 hybrids bred from A/J mice which develop chronic myocarditis and C57BL/6J mice which resolve the virus-induced lesions. Previous mouse studies demonstrated that the prevalence of heart-specific autoantibodies varied with the H-2 complex. However, in 25 H-2 congenic mouse strains the strain background was the predominant determinant of autoantibody presence. Recently, we extended our genetic evaluation of the chromosomal locations governing autoantibody responses by examining 25 AXB and BXA recombinant inbred strains. Two populations of heart-specific autoantibodies were demonstrated against sarcolemmal and cardiac myosin antigens. Analyses of the AXB/BXA strain distribution patterns for these two traits revealed that the anti-sarcolemmal response was controlled by a gene(s) linked to Np-2 and Ter alpha loci on chromosome 14. Linkage could not be assigned for the anti-cardiac myosin response."	Clin Exp Immunol	1991	Nov	"Traystman MD, Beisel KW."	1657464	2 weeks	both		Values determined using a myosin ELISA	640	1280	80	40	160	320			160	320	80			80					160	320	160	80	320	160		320		640					320		320		320	160	160							160			160	160	320	160		Nathan Copeland
Production of cardiac myosin in Coxackie virus B3- infected AXB/BXA  mice	% residual activity after absorption of  heart	Genetic control of Coxsackievirus B3-induced heart-specific autoantibodies associated with chronic myocarditis.	"Cardiac-specific autoantibodies to sarcolemmal and cardiac myosin antigens observed during the chronic phase of Coxsackievirus B3-induced myocarditis appear to be under autosomal recessive control. This observation is based on examination of F1 hybrids bred from A/J mice which develop chronic myocarditis and C57BL/6J mice which resolve the virus-induced lesions. Previous mouse studies demonstrated that the prevalence of heart-specific autoantibodies varied with the H-2 complex. However, in 25 H-2 congenic mouse strains the strain background was the predominant determinant of autoantibody presence. Recently, we extended our genetic evaluation of the chromosomal locations governing autoantibody responses by examining 25 AXB and BXA recombinant inbred strains. Two populations of heart-specific autoantibodies were demonstrated against sarcolemmal and cardiac myosin antigens. Analyses of the AXB/BXA strain distribution patterns for these two traits revealed that the anti-sarcolemmal response was controlled by a gene(s) linked to Np-2 and Ter alpha loci on chromosome 14. Linkage could not be assigned for the anti-cardiac myosin response."	Clin Exp Immunol	1991	Nov	"Traystman MD, Beisel KW."	1657464	2 weeks	both			27	38	0	0	0	44			0	21									0	26	13			0		25		32					0		0		0		0							0			0	27	36	36		Nathan Copeland
Production of cardiac myosin in Coxackie virus B3- infected AXB/BXA  mice	% residual activity after absorption of skeletal	Genetic control of Coxsackievirus B3-induced heart-specific autoantibodies associated with chronic myocarditis.	"Cardiac-specific autoantibodies to sarcolemmal and cardiac myosin antigens observed during the chronic phase of Coxsackievirus B3-induced myocarditis appear to be under autosomal recessive control. This observation is based on examination of F1 hybrids bred from A/J mice which develop chronic myocarditis and C57BL/6J mice which resolve the virus-induced lesions. Previous mouse studies demonstrated that the prevalence of heart-specific autoantibodies varied with the H-2 complex. However, in 25 H-2 congenic mouse strains the strain background was the predominant determinant of autoantibody presence. Recently, we extended our genetic evaluation of the chromosomal locations governing autoantibody responses by examining 25 AXB and BXA recombinant inbred strains. Two populations of heart-specific autoantibodies were demonstrated against sarcolemmal and cardiac myosin antigens. Analyses of the AXB/BXA strain distribution patterns for these two traits revealed that the anti-sarcolemmal response was controlled by a gene(s) linked to Np-2 and Ter alpha loci on chromosome 14. Linkage could not be assigned for the anti-cardiac myosin response."	Clin Exp Immunol	1991	Nov	"Traystman MD, Beisel KW."	1657464	2 weeks	both			0	0	0	0	0	0			0	0									0	0	0			0		0		0					0		0		0		0							0			0	0	0	0		Nathan Copeland
Production of cardiac myosin in Coxackie virus B3- infected AXB/BXA  mice	Anti cardiac myosin phenotype	Genetic control of Coxsackievirus B3-induced heart-specific autoantibodies associated with chronic myocarditis.	"Cardiac-specific autoantibodies to sarcolemmal and cardiac myosin antigens observed during the chronic phase of Coxsackievirus B3-induced myocarditis appear to be under autosomal recessive control. This observation is based on examination of F1 hybrids bred from A/J mice which develop chronic myocarditis and C57BL/6J mice which resolve the virus-induced lesions. Previous mouse studies demonstrated that the prevalence of heart-specific autoantibodies varied with the H-2 complex. However, in 25 H-2 congenic mouse strains the strain background was the predominant determinant of autoantibody presence. Recently, we extended our genetic evaluation of the chromosomal locations governing autoantibody responses by examining 25 AXB and BXA recombinant inbred strains. Two populations of heart-specific autoantibodies were demonstrated against sarcolemmal and cardiac myosin antigens. Analyses of the AXB/BXA strain distribution patterns for these two traits revealed that the anti-sarcolemmal response was controlled by a gene(s) linked to Np-2 and Ter alpha loci on chromosome 14. Linkage could not be assigned for the anti-cardiac myosin response."	Clin Exp Immunol	1991	Nov	"Traystman MD, Beisel KW."	1657464	2 weeks	both		A denotes the A/J parental trait and B denotes the trait of C57Bl/6J	A	A	B	B	B	A			B	A									B	A	A			B		A		A					B		A		A		B							B			B	A	A	A		Nathan Copeland
Genetic relationsip between AXB/BXA recombinant inbred strains for anti- cardiac sarcolemmal antibody (ASA. cardiac myosin specific autoantibodies and Coxaskievirus B3- induced chronic myocarditis	H-2	Genetic control of Coxsackievirus B3-induced heart-specific autoantibodies associated with chronic myocarditis.	"Cardiac-specific autoantibodies to sarcolemmal and cardiac myosin antigens observed during the chronic phase of Coxsackievirus B3-induced myocarditis appear to be under autosomal recessive control. This observation is based on examination of F1 hybrids bred from A/J mice which develop chronic myocarditis and C57BL/6J mice which resolve the virus-induced lesions. Previous mouse studies demonstrated that the prevalence of heart-specific autoantibodies varied with the H-2 complex. However, in 25 H-2 congenic mouse strains the strain background was the predominant determinant of autoantibody presence. Recently, we extended our genetic evaluation of the chromosomal locations governing autoantibody responses by examining 25 AXB and BXA recombinant inbred strains. Two populations of heart-specific autoantibodies were demonstrated against sarcolemmal and cardiac myosin antigens. Analyses of the AXB/BXA strain distribution patterns for these two traits revealed that the anti-sarcolemmal response was controlled by a gene(s) linked to Np-2 and Ter alpha loci on chromosome 14. Linkage could not be assigned for the anti-cardiac myosin response."	Clin Exp Immunol	1991	Nov	"Traystman MD, Beisel KW."	1657464	2 weeks	both			a	b	b	a	a	a			a	b	a	a		b					a	a	b	b		a		b		a					a		b		b	b	a							b	B			a		a		Nathan Copeland
Genetic relationsip between AXB/BXA recombinant inbred strains for anti- cardiac sarcolemmal antibody (ASA. cardiac myosin specific autoantibodies and Coxaskievirus B3- induced chronic myocarditis	Anti - cardiac myosin	Genetic control of Coxsackievirus B3-induced heart-specific autoantibodies associated with chronic myocarditis.	"Cardiac-specific autoantibodies to sarcolemmal and cardiac myosin antigens observed during the chronic phase of Coxsackievirus B3-induced myocarditis appear to be under autosomal recessive control. This observation is based on examination of F1 hybrids bred from A/J mice which develop chronic myocarditis and C57BL/6J mice which resolve the virus-induced lesions. Previous mouse studies demonstrated that the prevalence of heart-specific autoantibodies varied with the H-2 complex. However, in 25 H-2 congenic mouse strains the strain background was the predominant determinant of autoantibody presence. Recently, we extended our genetic evaluation of the chromosomal locations governing autoantibody responses by examining 25 AXB and BXA recombinant inbred strains. Two populations of heart-specific autoantibodies were demonstrated against sarcolemmal and cardiac myosin antigens. Analyses of the AXB/BXA strain distribution patterns for these two traits revealed that the anti-sarcolemmal response was controlled by a gene(s) linked to Np-2 and Ter alpha loci on chromosome 14. Linkage could not be assigned for the anti-cardiac myosin response."	Clin Exp Immunol	1991	Nov	"Traystman MD, Beisel KW."	1657464	2 weeks	both		A denotes the A/J parental trait and B denotes the trait of C57Bl/6J	A	A	B	B	B	A			B	B									B	A	A			B		A		A					B		B		B		B							B	B			A	A	A		Nathan Copeland
Genetic relationsip between AXB/BXA recombinant inbred strains for anti- cardiac sarcolemmal antibody (ASA. cardiac myosin specific autoantibodies and Coxaskievirus B3- induced chronic myocarditis	ASA	Genetic control of Coxsackievirus B3-induced heart-specific autoantibodies associated with chronic myocarditis.	"Cardiac-specific autoantibodies to sarcolemmal and cardiac myosin antigens observed during the chronic phase of Coxsackievirus B3-induced myocarditis appear to be under autosomal recessive control. This observation is based on examination of F1 hybrids bred from A/J mice which develop chronic myocarditis and C57BL/6J mice which resolve the virus-induced lesions. Previous mouse studies demonstrated that the prevalence of heart-specific autoantibodies varied with the H-2 complex. However, in 25 H-2 congenic mouse strains the strain background was the predominant determinant of autoantibody presence. Recently, we extended our genetic evaluation of the chromosomal locations governing autoantibody responses by examining 25 AXB and BXA recombinant inbred strains. Two populations of heart-specific autoantibodies were demonstrated against sarcolemmal and cardiac myosin antigens. Analyses of the AXB/BXA strain distribution patterns for these two traits revealed that the anti-sarcolemmal response was controlled by a gene(s) linked to Np-2 and Ter alpha loci on chromosome 14. Linkage could not be assigned for the anti-cardiac myosin response."	Clin Exp Immunol	1991	Nov	"Traystman MD, Beisel KW."	1657464	2 weeks	both		A denotes the A/J parental trait and B denotes the trait of C57Bl/6J	A	A	B	B		A			B	A	B			B					A	A	B	B	B	B		A		B					A		A		A	B								A	A			A	A	A		Nathan Copeland
Genetic relationsip between AXB/BXA recombinant inbred strains for anti- cardiac sarcolemmal antibody (ASA. cardiac myosin specific autoantibodies and Coxaskievirus B3- induced chronic myocarditis	Myocarditis	Genetic control of Coxsackievirus B3-induced heart-specific autoantibodies associated with chronic myocarditis.	"Cardiac-specific autoantibodies to sarcolemmal and cardiac myosin antigens observed during the chronic phase of Coxsackievirus B3-induced myocarditis appear to be under autosomal recessive control. This observation is based on examination of F1 hybrids bred from A/J mice which develop chronic myocarditis and C57BL/6J mice which resolve the virus-induced lesions. Previous mouse studies demonstrated that the prevalence of heart-specific autoantibodies varied with the H-2 complex. However, in 25 H-2 congenic mouse strains the strain background was the predominant determinant of autoantibody presence. Recently, we extended our genetic evaluation of the chromosomal locations governing autoantibody responses by examining 25 AXB and BXA recombinant inbred strains. Two populations of heart-specific autoantibodies were demonstrated against sarcolemmal and cardiac myosin antigens. Analyses of the AXB/BXA strain distribution patterns for these two traits revealed that the anti-sarcolemmal response was controlled by a gene(s) linked to Np-2 and Ter alpha loci on chromosome 14. Linkage could not be assigned for the anti-cardiac myosin response."	Clin Exp Immunol	1991	Nov	"Traystman MD, Beisel KW."	1657464	2 weeks	both		A denotes the A/J parental trait and B denotes the trait of C57Bl/6J	A	A	B	B	B	A			B	A	B			A					A	B	B	B	B	A		A		B					A		B		B	A	B							B	B			A	A	A		Nathan Copeland
"Quantitation of the Immunocytochemical distribution of corticosterone in the adrenal cortices of A/J, B6, and (BXA) hybrids and AXB and BXA RI lines"	Number of sectors ananlyzed	Genetic analysis of the distribution of corticosterone-containing cells in mouse adrenal cortex.	"Strains A/J and C57BL/6J (B6) differ in susceptibility to many neoplasms and infectious agents, with B6 mice generally being more resistant. Glucocorticoids protect against some of these pathologies. We examined the distribution of adrenocortical corticosterone (CS), the major endogenous glucocorticoid in mice, in these strains, using anti-CS serum. A distinct strain difference was found. B6 adrenals exhibited abundant CS-positive cells in cord-like arrays while A/J adrenals contained fewer, randomly arranged CS-positive cells. To quantify these results, each adrenal cortex was divided into eight sectors and each sector was classified as to phenotype. Ninety-three percent of the sectors of B6 cortices exhibited the cord-like pattern, whereas only 15% of the sectors of A/J cortices exhibited this pattern. These differences are consistent with a hypothesis that A/J mice are relatively deficient in the prophylactic activities of endogenous glucocorticoids. Adrenal glands from (C57BL/6J x A/J)F1 hybrid mice had approximately equal proportions of areas exhibiting each phenotype, indicating codominant alleles for this trait. We propose the name Cor for this gene. Thirty AXB and BXA recombinant inbred (RI) lines of mice derived from A/J and B6 progenitors were examined for CS immunostaining. Twenty-eight of them had either predominantly A/J-like or predominantly B6-like phenotypes. These RI data support either of two hypotheses. Hypothesis 1 emphasizes the nearly complete concordance of the RI lines with progenitor phenotypes and proposes that a single Cor gene regulates the distribution of CS-positive cells. Using this model, the strain distribution among RI lines implies linkage of Cor to a region on chromosome 6, 27-37 cM from the centromere. Hypothesis 2, which gives greater weight to the two RI lines with intermediate numbers of CS-positive cells, postulates an epistatic interaction between two Cor loci."	Proc Soc Exp Biol Med	1990	June	"Thaete LG, Nesbitt MN, Malkinson AM."	2349252	8 weeks	male			40		40		8	16	32	95	51	32	37	32	62	64		32	12		40	38	36						24	40	16			64		24	40	44	39	36	32	46	40					40					22	52		Nathan Copeland
"Quantitation of the Immunocytochemical distribution of corticosterone in the adrenal cortices of A/J, B6, and (BXA) hybrids and AXB and BXA RI lines"	Percentage of B6-like patterns	Genetic analysis of the distribution of corticosterone-containing cells in mouse adrenal cortex.	"Strains A/J and C57BL/6J (B6) differ in susceptibility to many neoplasms and infectious agents, with B6 mice generally being more resistant. Glucocorticoids protect against some of these pathologies. We examined the distribution of adrenocortical corticosterone (CS), the major endogenous glucocorticoid in mice, in these strains, using anti-CS serum. A distinct strain difference was found. B6 adrenals exhibited abundant CS-positive cells in cord-like arrays while A/J adrenals contained fewer, randomly arranged CS-positive cells. To quantify these results, each adrenal cortex was divided into eight sectors and each sector was classified as to phenotype. Ninety-three percent of the sectors of B6 cortices exhibited the cord-like pattern, whereas only 15% of the sectors of A/J cortices exhibited this pattern. These differences are consistent with a hypothesis that A/J mice are relatively deficient in the prophylactic activities of endogenous glucocorticoids. Adrenal glands from (C57BL/6J x A/J)F1 hybrid mice had approximately equal proportions of areas exhibiting each phenotype, indicating codominant alleles for this trait. We propose the name Cor for this gene. Thirty AXB and BXA recombinant inbred (RI) lines of mice derived from A/J and B6 progenitors were examined for CS immunostaining. Twenty-eight of them had either predominantly A/J-like or predominantly B6-like phenotypes. These RI data support either of two hypotheses. Hypothesis 1 emphasizes the nearly complete concordance of the RI lines with progenitor phenotypes and proposes that a single Cor gene regulates the distribution of CS-positive cells. Using this model, the strain distribution among RI lines implies linkage of Cor to a region on chromosome 6, 27-37 cM from the centromere. Hypothesis 2, which gives greater weight to the two RI lines with intermediate numbers of CS-positive cells, postulates an epistatic interaction between two Cor loci."	Proc Soc Exp Biol Med	1990	June	"Thaete LG, Nesbitt MN, Malkinson AM."	2349252	8 weeks	male			15		90		25	75	3	84	29	31	24	91	84	20		3	50		75	58	83						100	83	19			14		33	18	18	15	89	22	17	3					83					73	98		Nathan Copeland
Segregation of Chromosome 2 Loci AXB and BXA recombinant inbred mice	Neb	"A new sodium channel alpha-subunit gene (Scn9a) from Schwann cells maps to the Scn1a, Scn2a, Scn3a cluster of mouse chromosome 2."	"We have used a total of 27 AXB/BXA recombinant inbred mouse strains to determine the chromosomal location of a newly identified gene encoding an alpha-subunit isoform of the sodium channel from Schwann cells, Scn9a. Linkage analysis established that Scn9a mapped to the proximal segment of mouse chromosome 2. The segregation of restriction fragment length polymorphisms in 145 progeny from a Mus spretus x C57BL/6J backcross indicates that Scn9a is very tightly linked to Scn1a (gene encoding the type I sodium channel alpha-subunit of the brain) and forms part of a cluster of four Scna genes located on mouse chromosome 2."	Genomics 	1996	Aug	"Beckers MC, Ernst E, Belcher S, Howe J, Levenson R, Gros P."	8812438				Strain specific alleles are abbreviated as B (C57Cl/6J) and A  (A/J)					B	A	A	A	A	A	A	A	B	B	B	B	A	A	A	A	B	B	A	A		A	A		B	B		B		B	B	A			B		A		A	B	B		A		B	A	B			Nathan Copeland
Segregation of Chromosome 2 Loci AXB and BXA recombinant inbred mice	D2J3	"A new sodium channel alpha-subunit gene (Scn9a) from Schwann cells maps to the Scn1a, Scn2a, Scn3a cluster of mouse chromosome 2."	"We have used a total of 27 AXB/BXA recombinant inbred mouse strains to determine the chromosomal location of a newly identified gene encoding an alpha-subunit isoform of the sodium channel from Schwann cells, Scn9a. Linkage analysis established that Scn9a mapped to the proximal segment of mouse chromosome 2. The segregation of restriction fragment length polymorphisms in 145 progeny from a Mus spretus x C57BL/6J backcross indicates that Scn9a is very tightly linked to Scn1a (gene encoding the type I sodium channel alpha-subunit of the brain) and forms part of a cluster of four Scna genes located on mouse chromosome 2."	Genomics 	1996	Aug	"Beckers MC, Ernst E, Belcher S, Howe J, Levenson R, Gros P."	8812438				Strain specific alleles are abbreviated as B (C57Cl/6J) and A  (A/J)					B	A	B	A	A	A	B	A	A	B	B	B	B	B	A	B	B	B	B	A		A	B		B	A		B		B	A	A		A	A	A	A		B	A	B		A		B	B	B	A	A	Nathan Copeland
Segregation of Chromosome 2 Loci AXB and BXA recombinant inbred mice	Scn9a	"A new sodium channel alpha-subunit gene (Scn9a) from Schwann cells maps to the Scn1a, Scn2a, Scn3a cluster of mouse chromosome 2."	"We have used a total of 27 AXB/BXA recombinant inbred mouse strains to determine the chromosomal location of a newly identified gene encoding an alpha-subunit isoform of the sodium channel from Schwann cells, Scn9a. Linkage analysis established that Scn9a mapped to the proximal segment of mouse chromosome 2. The segregation of restriction fragment length polymorphisms in 145 progeny from a Mus spretus x C57BL/6J backcross indicates that Scn9a is very tightly linked to Scn1a (gene encoding the type I sodium channel alpha-subunit of the brain) and forms part of a cluster of four Scna genes located on mouse chromosome 2."	Genomics 	1996	Aug	"Beckers MC, Ernst E, Belcher S, Howe J, Levenson R, Gros P."	8812438				Strain specific alleles are abbreviated as B (C57Cl/6J) and A  (A/J)					B	A		A	A	A		A		B	B		B	B				B	B			A			B	A		B		B	A			A	A	A	A		B	A							B	A	A	Nathan Copeland
Segregation of Chromosome 2 Loci AXB and BXA recombinant inbred mice	D2Mit14	"A new sodium channel alpha-subunit gene (Scn9a) from Schwann cells maps to the Scn1a, Scn2a, Scn3a cluster of mouse chromosome 2."	"We have used a total of 27 AXB/BXA recombinant inbred mouse strains to determine the chromosomal location of a newly identified gene encoding an alpha-subunit isoform of the sodium channel from Schwann cells, Scn9a. Linkage analysis established that Scn9a mapped to the proximal segment of mouse chromosome 2. The segregation of restriction fragment length polymorphisms in 145 progeny from a Mus spretus x C57BL/6J backcross indicates that Scn9a is very tightly linked to Scn1a (gene encoding the type I sodium channel alpha-subunit of the brain) and forms part of a cluster of four Scna genes located on mouse chromosome 2."	Genomics 	1996	Aug	"Beckers MC, Ernst E, Belcher S, Howe J, Levenson R, Gros P."	8812438				Strain specific alleles are abbreviated as B (C57Cl/6J) and A  (A/J)					B	A	B	A	A	A	B	A	A	B	B	A	B	B	A	B	B	B	B	A		A	A		B	A		B		B	A	A		A	A	A	A		B	A	B		A		B	B	B	A	B	Nathan Copeland
AXB/BXA RI strain distribution pattern for susceptibility to CVB-3 induced mycarditis in Mice	H - 2 haplotype	Susceptibility to Coxsackievirus B3-induced chronic myocarditis maps near the murine Tcr alpha and Myhc alpha loci on chromosome 14.	"This study was undertaken to determine the genetic control of host susceptibility to coxsackievirus B3 (CVB3)-induced chronic myocarditis in a mouse model. An autosomal recessive autoimmune myocardial disease (amd) gene (possibly more than one gene), which determined susceptibility to CVB3-induced chronic myocarditis in the A/J and DBA/2J inbred mouse strains, was mapped to a segment of chromosome 14. Data from both the AXB/BXA recombinant inbred (RI) strains and the B10.D2(57N) H-8b congenic mice supported this linkage relationship. Analysis of the AXB/BXA RI strain distribution patterns suggested that amd maps distal to the Np-2, Tcr alpha, and Myhc alpha loci."	Am J Pathol	1991	Mar	"Traystman MD, Chow LH, McManus BM, Herskowitz A, Nesbitt MN, Beisel KW."	1848043	2 weeks				a	b	b	a	a	a			b	b	a	a		b					a	a	b	b		a		b		a					a		b		b	b	a							b			b	a		a		Nathan Copeland
AXB/BXA RI strain distribution pattern for susceptibility to CVB-3 induced mycarditis in Mice	Fibrocalcitic lesions:   Prevalence	Susceptibility to Coxsackievirus B3-induced chronic myocarditis maps near the murine Tcr alpha and Myhc alpha loci on chromosome 14.	"This study was undertaken to determine the genetic control of host susceptibility to coxsackievirus B3 (CVB3)-induced chronic myocarditis in a mouse model. An autosomal recessive autoimmune myocardial disease (amd) gene (possibly more than one gene), which determined susceptibility to CVB3-induced chronic myocarditis in the A/J and DBA/2J inbred mouse strains, was mapped to a segment of chromosome 14. Data from both the AXB/BXA recombinant inbred (RI) strains and the B10.D2(57N) H-8b congenic mice supported this linkage relationship. Analysis of the AXB/BXA RI strain distribution patterns suggested that amd maps distal to the Np-2, Tcr alpha, and Myhc alpha loci."	Am J Pathol	1991	Mar	"Traystman MD, Chow LH, McManus BM, Herskowitz A, Nesbitt MN, Beisel KW."	1848043	2 weeks			Expressed as the number of positive animals/total number and the percentage of animals showing pathology is after the hyphen	20/50 - 40	50/122 - 41	13/91 - 14	7/61 -11	1/11/09	15/21 - 71			14/29 - 48	14/15 - 93 	8/18/44	0/11 - 0		6/11/55					16/19 - 84	6/30/20	1/23/04	5/25/20	0/19 - 0	12/25/48		10/10 - 100		11/22/50					3/10/30		0/7 - 0		3/17/18	8/16/50	0/18 - 0							9/28/32			11/20/55	11/20/55	3/13/23	3/28/11		Nathan Copeland
AXB/BXA RI strain distribution pattern for susceptibility to CVB-3 induced mycarditis in Mice	Fibrocalcitic lesions:   PI	Susceptibility to Coxsackievirus B3-induced chronic myocarditis maps near the murine Tcr alpha and Myhc alpha loci on chromosome 14.	"This study was undertaken to determine the genetic control of host susceptibility to coxsackievirus B3 (CVB3)-induced chronic myocarditis in a mouse model. An autosomal recessive autoimmune myocardial disease (amd) gene (possibly more than one gene), which determined susceptibility to CVB3-induced chronic myocarditis in the A/J and DBA/2J inbred mouse strains, was mapped to a segment of chromosome 14. Data from both the AXB/BXA recombinant inbred (RI) strains and the B10.D2(57N) H-8b congenic mice supported this linkage relationship. Analysis of the AXB/BXA RI strain distribution patterns suggested that amd maps distal to the Np-2, Tcr alpha, and Myhc alpha loci."	Am J Pathol	1991	Mar	"Traystman MD, Chow LH, McManus BM, Herskowitz A, Nesbitt MN, Beisel KW."	1848043	2 weeks			The mean score based on a scale of 0 to  4. Pathology scores were given by two or three independent observers 	1.5	1.2	0.2	0.1	0.1	1.7			0.8	2.2	0.5	0		1					1.8	0.3	0.2	0.4	0	1		2.4		0.6					0.4		0		0.2	1.1	0							0.5			0.9	1.4	0.8	0.2		Nathan Copeland
AXB/BXA RI strain distribution pattern for susceptibility to CVB-3 induced mycarditis in Mice	Chronic mycocarditis:  Prevalence 	Susceptibility to Coxsackievirus B3-induced chronic myocarditis maps near the murine Tcr alpha and Myhc alpha loci on chromosome 14.	"This study was undertaken to determine the genetic control of host susceptibility to coxsackievirus B3 (CVB3)-induced chronic myocarditis in a mouse model. An autosomal recessive autoimmune myocardial disease (amd) gene (possibly more than one gene), which determined susceptibility to CVB3-induced chronic myocarditis in the A/J and DBA/2J inbred mouse strains, was mapped to a segment of chromosome 14. Data from both the AXB/BXA recombinant inbred (RI) strains and the B10.D2(57N) H-8b congenic mice supported this linkage relationship. Analysis of the AXB/BXA RI strain distribution patterns suggested that amd maps distal to the Np-2, Tcr alpha, and Myhc alpha loci."	Am J Pathol	1991	Mar	"Traystman MD, Chow LH, McManus BM, Herskowitz A, Nesbitt MN, Beisel KW."	1848043	2 weeks			Expressed as the number of positive animals/total number and the percentage of animals showing pathology is after the hyphen	9/50 - 18	19/122 - 16	1/91 - 1	0/61 - 0	1/11/09	10/21 - 48`			0/29 - 0	7/15/47	0/18 - 0	0/11 - 0		4/11/36					3/19/16	0/30 - 0	0/23 - 0	0/25 - 0	0/19 - 0	7/25/28		4/10/40		0/22 -0					3/10/30		0/7 - 0		0/17 - 0	2/16/13	0/18 - 0							0/28 - 0			0/20 - 0	5/20/25	2/13/15	1/28/04		Nathan Copeland
AXB/BXA RI strain distribution pattern for susceptibility to CVB-3 induced mycarditis in Mice	Chronic mycarditis:  Phenotype	Susceptibility to Coxsackievirus B3-induced chronic myocarditis maps near the murine Tcr alpha and Myhc alpha loci on chromosome 14.	"This study was undertaken to determine the genetic control of host susceptibility to coxsackievirus B3 (CVB3)-induced chronic myocarditis in a mouse model. An autosomal recessive autoimmune myocardial disease (amd) gene (possibly more than one gene), which determined susceptibility to CVB3-induced chronic myocarditis in the A/J and DBA/2J inbred mouse strains, was mapped to a segment of chromosome 14. Data from both the AXB/BXA recombinant inbred (RI) strains and the B10.D2(57N) H-8b congenic mice supported this linkage relationship. Analysis of the AXB/BXA RI strain distribution patterns suggested that amd maps distal to the Np-2, Tcr alpha, and Myhc alpha loci."	Am J Pathol	1991	Mar	"Traystman MD, Chow LH, McManus BM, Herskowitz A, Nesbitt MN, Beisel KW."	1848043	2 weeks			Strains were classified as susceptible (s) or resistent (r) to chronic myocarditis as determined by chi - square analyses (P= 0.05) using the prevalence of disease observed in the H-2 haplotype-matched parental strains as the expected values	s	s	r	r	r	s			r	s	r	r		s					s	r	r	r	r	s		s		r					s		r		r	s	r							r			r	s	s	s		Nathan Copeland
Dissociation of IL 1 production and of tumor cytotoxicity by macrophanges from AXB/BXA  RIstrains	IL 1 Phenotype	Genetic regulation of lipopolysaccharide-induced interleukin 1 production by murine peritoneal macrophages.	"The production of IL 1 by LPS-stimulated peritoneal macrophages from inbred mouse strains was studied. Macrophages from A/J (A) mice were deficient in IL 1 production, when compared with high IL 1-producing strains, including C57BL/6J (B). The difference between A and B macrophages was maintained over a wide LPS concentration range and throughout a 72-hr incubation period. Because of these differences, it was possible to investigate the mechanisms regulating IL 1 production by applying techniques of genetic analysis by using recombinant inbred (RI) strains derived from the A and B progenitors. A strain distribution pattern (SDP) of IL 1 production (low/high response) was obtained with the use of 15 AXB/BXA RI strains. This suggested the presence of a major gene locus controlling the production of IL 1 in response to LPS stimulation, with allelic differences presumably resulting in deficient or efficient IL 1 production. In addition, there appeared to be one or more other loci involved in determining the magnitude of the IL 1 response to LPS in the responder mice. The IL 1 response did not appear to be linked to the major histocompatibility complex, since B10.A mice (which share the same H-2a haplotype as A/J) were efficient IL 1 producers. There did not appear to be any correlation between the degree of IL 1 production and the magnitude of the peritoneal macrophage inflammatory response, or between IL 1 production and LPS responsiveness (as determined by splenocyte proliferation). SDP analysis also indicated that the IL 1 response was not linked to macrophage tumoricidal activity. A comparison of the SDP for IL 1 production with a library of SDP for other known genetic waits suggested linkage with at least four loci on chromosome 1."	J Immunol	1987	June	"Brandwein SR, Skamene E, Aubut JA, Gervais F, Nesbitt MN."	3495586	6 to 8 weeks	males	5-Mar	A = defective; B = effective 	A		B		A			A		A	A									A													B		A																			Nathan Copeland
Dissociation of IL 1 production and of tumor cytotoxicity by macrophanges from AXB/BXA  RIstrains	Tumoricidal Phenotype	Genetic regulation of lipopolysaccharide-induced interleukin 1 production by murine peritoneal macrophages.	"The production of IL 1 by LPS-stimulated peritoneal macrophages from inbred mouse strains was studied. Macrophages from A/J (A) mice were deficient in IL 1 production, when compared with high IL 1-producing strains, including C57BL/6J (B). The difference between A and B macrophages was maintained over a wide LPS concentration range and throughout a 72-hr incubation period. Because of these differences, it was possible to investigate the mechanisms regulating IL 1 production by applying techniques of genetic analysis by using recombinant inbred (RI) strains derived from the A and B progenitors. A strain distribution pattern (SDP) of IL 1 production (low/high response) was obtained with the use of 15 AXB/BXA RI strains. This suggested the presence of a major gene locus controlling the production of IL 1 in response to LPS stimulation, with allelic differences presumably resulting in deficient or efficient IL 1 production. In addition, there appeared to be one or more other loci involved in determining the magnitude of the IL 1 response to LPS in the responder mice. The IL 1 response did not appear to be linked to the major histocompatibility complex, since B10.A mice (which share the same H-2a haplotype as A/J) were efficient IL 1 producers. There did not appear to be any correlation between the degree of IL 1 production and the magnitude of the peritoneal macrophage inflammatory response, or between IL 1 production and LPS responsiveness (as determined by splenocyte proliferation). SDP analysis also indicated that the IL 1 response was not linked to macrophage tumoricidal activity. A comparison of the SDP for IL 1 production with a library of SDP for other known genetic waits suggested linkage with at least four loci on chromosome 1."	J Immunol	1987	June	"Brandwein SR, Skamene E, Aubut JA, Gervais F, Nesbitt MN."	3495586	6 to 8 weeks	males	5-Mar	A = defective; B = effective 	A		B		B			A		A	A									B													A		B																			Nathan Copeland
Mean survival time of AXB/BXA RI mice to plasmodium chabaudi	susceptible or resistant	Murine malaria: resistance of AXB/BXA recombinant inbred mice to Plasmodium chabaudi.	"The level of resistance to infection with Plasmodium chabaudi is genetically controlled. We have previously reported that a single dominant gene is responsible for the variation in host resistance to malaria between susceptible A/J- and resistant C57BL-derived mice. In the present study, recombinant inbred strain analysis was performed with AXB/BXA recombinant inbred strains derived from A/J and C57BL/6 progenitors. Typing of 17 AXB/BXA recombinant inbred strains confirmed the unigenic control of inheritance in this particular strain combination and allowed us to demonstrate genetic linkage between the traits of resistance (defined as a prolonged survival and a low peak parasitemia) and the magnitude of splenomegaly. The influence of sex on the course of infection, which we previously reported in the examination of segregating populations (Stevenson et al., Infect. Immun. 38:80-88, 1982), was again demonstrated in the survey of RI strains."	Infect Immun	1985	Feb	"Stevenson MM, Skamene E."	3967923	6 to 8 weeks			s = susceptibler = resistant	s	r			s	r	r	s	r	r	r	r	s			s				r									r				s		r				s	r	r													Nathan Copeland
Mean survival time of AXB/BXA RI mice  to plasmodium chabaudi	Mean survival time	Murine malaria: resistance of AXB/BXA recombinant inbred mice to Plasmodium chabaudi.	"The level of resistance to infection with Plasmodium chabaudi is genetically controlled. We have previously reported that a single dominant gene is responsible for the variation in host resistance to malaria between susceptible A/J- and resistant C57BL-derived mice. In the present study, recombinant inbred strain analysis was performed with AXB/BXA recombinant inbred strains derived from A/J and C57BL/6 progenitors. Typing of 17 AXB/BXA recombinant inbred strains confirmed the unigenic control of inheritance in this particular strain combination and allowed us to demonstrate genetic linkage between the traits of resistance (defined as a prolonged survival and a low peak parasitemia) and the magnitude of splenomegaly. The influence of sex on the course of infection, which we previously reported in the examination of segregating populations (Stevenson et al., Infect. Immun. 38:80-88, 1982), was again demonstrated in the survey of RI strains."	Infect Immun	1985	Feb	"Stevenson MM, Skamene E."	3967923	6 to 8 weeks			average first then days in parenteses	9.8 (7 - 14)		>14		10.6 (9 - 15)	>14	>14	10.1  (9 - 14)	>14	>14	>14	>14	7.0 (7 - 10)			7.7 (7 - 10)				>14									>14				9.7  (7 - 10)		>14				8.6  (10 - 12)	>14	>14													Nathan Copeland
Peak parasitemia and spleen weights in male and gemale AXB/BXA RI strains	Peak parasitemia in males	Murine malaria: resistance of AXB/BXA recombinant inbred mice to Plasmodium chabaudi.	"The level of resistance to infection with Plasmodium chabaudi is genetically controlled. We have previously reported that a single dominant gene is responsible for the variation in host resistance to malaria between susceptible A/J- and resistant C57BL-derived mice. In the present study, recombinant inbred strain analysis was performed with AXB/BXA recombinant inbred strains derived from A/J and C57BL/6 progenitors. Typing of 17 AXB/BXA recombinant inbred strains confirmed the unigenic control of inheritance in this particular strain combination and allowed us to demonstrate genetic linkage between the traits of resistance (defined as a prolonged survival and a low peak parasitemia) and the magnitude of splenomegaly. The influence of sex on the course of infection, which we previously reported in the examination of segregating populations (Stevenson et al., Infect. Immun. 38:80-88, 1982), was again demonstrated in the survey of RI strains."	Infect Immun	1985	Feb	"Stevenson MM, Skamene E."	3967923	6 to 8 weeks			%									41.7							58.4				38.5													63.2																					Nathan Copeland
Peak parasitemia and spleen weights in male and gemale AXB/BXA RI strains	Peak parasitemia in females	Murine malaria: resistance of AXB/BXA recombinant inbred mice to Plasmodium chabaudi.	"The level of resistance to infection with Plasmodium chabaudi is genetically controlled. We have previously reported that a single dominant gene is responsible for the variation in host resistance to malaria between susceptible A/J- and resistant C57BL-derived mice. In the present study, recombinant inbred strain analysis was performed with AXB/BXA recombinant inbred strains derived from A/J and C57BL/6 progenitors. Typing of 17 AXB/BXA recombinant inbred strains confirmed the unigenic control of inheritance in this particular strain combination and allowed us to demonstrate genetic linkage between the traits of resistance (defined as a prolonged survival and a low peak parasitemia) and the magnitude of splenomegaly. The influence of sex on the course of infection, which we previously reported in the examination of segregating populations (Stevenson et al., Infect. Immun. 38:80-88, 1982), was again demonstrated in the survey of RI strains."	Infect Immun	1985	Feb	"Stevenson MM, Skamene E."	3967923	6 to 8 weeks			%									39.1							51.2				36.8													64.1																					Nathan Copeland
Peak parasitemia and spleen weights in male and gemale AXB/BXA RI strains	spleen weight  in males	Murine malaria: resistance of AXB/BXA recombinant inbred mice to Plasmodium chabaudi.	"The level of resistance to infection with Plasmodium chabaudi is genetically controlled. We have previously reported that a single dominant gene is responsible for the variation in host resistance to malaria between susceptible A/J- and resistant C57BL-derived mice. In the present study, recombinant inbred strain analysis was performed with AXB/BXA recombinant inbred strains derived from A/J and C57BL/6 progenitors. Typing of 17 AXB/BXA recombinant inbred strains confirmed the unigenic control of inheritance in this particular strain combination and allowed us to demonstrate genetic linkage between the traits of resistance (defined as a prolonged survival and a low peak parasitemia) and the magnitude of splenomegaly. The influence of sex on the course of infection, which we previously reported in the examination of segregating populations (Stevenson et al., Infect. Immun. 38:80-88, 1982), was again demonstrated in the survey of RI strains."	Infect Immun	1985	Feb	"Stevenson MM, Skamene E."	3967923	6 to 8 weeks			mg									547							420				652													395																					Nathan Copeland
Peak parasitemia and spleen weights in male and gemale AXB/BXA RI strains	spleen weight in females	Murine malaria: resistance of AXB/BXA recombinant inbred mice to Plasmodium chabaudi.	"The level of resistance to infection with Plasmodium chabaudi is genetically controlled. We have previously reported that a single dominant gene is responsible for the variation in host resistance to malaria between susceptible A/J- and resistant C57BL-derived mice. In the present study, recombinant inbred strain analysis was performed with AXB/BXA recombinant inbred strains derived from A/J and C57BL/6 progenitors. Typing of 17 AXB/BXA recombinant inbred strains confirmed the unigenic control of inheritance in this particular strain combination and allowed us to demonstrate genetic linkage between the traits of resistance (defined as a prolonged survival and a low peak parasitemia) and the magnitude of splenomegaly. The influence of sex on the course of infection, which we previously reported in the examination of segregating populations (Stevenson et al., Infect. Immun. 38:80-88, 1982), was again demonstrated in the survey of RI strains."	Infect Immun	1985	Feb	"Stevenson MM, Skamene E."	3967923	6 to 8 weeks			mg									510							430				568													251																					Nathan Copeland
Relationship between susceptibility/ resistance to MAIDS and the mouse MHC	Phenotype to LP - BM5:  Pathology	Susceptibility to a mouse acquired immunodeficiency syndrome is influenced by the H-2.	"The development of a mouse acquired immunodeficiency syndrome (MAIDS) induced following LP-BM5 MuLV infection depends on host genetic factors. Susceptible mice, such as C57BL/6J mice, develop a profound impairment of lymphoproliferative response to mitogens and hyperplasia of lymphoid organs and succumb to infection within 6 months. These changes do not occur in resistant mice, such as A/J mice. Resistance to MAIDS is a dominant trait since (C57BL/6J x A/J)F1 hybrid mice did not develop any immune dysfunctions following infection. Genetic regulation of the trait of resistance/susceptibility to MAIDS was determined in AXB/BXA recombinant inbred (RI) mouse strains (derived from resistant A/J and susceptible C57BL/6J progenitors). Two different criteria were used to determine their resistance or susceptibility to developing MAIDS: the gross pathologic evaluation of lymphoid organs at 13-15 weeks of infection, and survival. RI mouse strains segregated into two non-overlapping groups. The first group did not develop any significant pathology, and these mouse strains were considered as resistant to MAIDS. The second group showed the virus-induced pathological changes as well as an immunological dysfunction as seen in C57BL/6J progenitor mice, and these strains were thus considered as susceptible to MAIDS. This bimodal strain distribution pattern of resistance/susceptibility to MAIDS among the RI strains suggests that this phenotype is controlled by a single gene. Linkage analysis with other allelic markers showed a strong association between resistance/susceptibility to MAIDS and the H-2 complex. Possession of the H-2b haplotype derived from C57BL/6J mice was associated with susceptibility to MAIDS, while the H-2a haplotype conferred resistance to the disease. This finding was confirmed by demonstrating that H-2a congenics on the susceptible C57BL/10 background were as resistant to MAIDS as A/J mice which donated the H-2a locus. Gene(s) within the H-2 complex thus represent the major regulatory mechanism of resistance/susceptibility to MAIDS."	Immunogenetics	1989		"Hamelin-Bourassa D, Skamene E, Gervais F."	2551819	8 - 12 weeks			s = susceptibler = resistant	r		s			r								s						r	s	s		r				r		s		r			r	r	s			s						r			s					Nathan Copeland
Relationship between susceptibility/ resistance to MAIDS and the mouse MHC	Phenotype to LP - BM5:  Survival 	Susceptibility to a mouse acquired immunodeficiency syndrome is influenced by the H-2.	"The development of a mouse acquired immunodeficiency syndrome (MAIDS) induced following LP-BM5 MuLV infection depends on host genetic factors. Susceptible mice, such as C57BL/6J mice, develop a profound impairment of lymphoproliferative response to mitogens and hyperplasia of lymphoid organs and succumb to infection within 6 months. These changes do not occur in resistant mice, such as A/J mice. Resistance to MAIDS is a dominant trait since (C57BL/6J x A/J)F1 hybrid mice did not develop any immune dysfunctions following infection. Genetic regulation of the trait of resistance/susceptibility to MAIDS was determined in AXB/BXA recombinant inbred (RI) mouse strains (derived from resistant A/J and susceptible C57BL/6J progenitors). Two different criteria were used to determine their resistance or susceptibility to developing MAIDS: the gross pathologic evaluation of lymphoid organs at 13-15 weeks of infection, and survival. RI mouse strains segregated into two non-overlapping groups. The first group did not develop any significant pathology, and these mouse strains were considered as resistant to MAIDS. The second group showed the virus-induced pathological changes as well as an immunological dysfunction as seen in C57BL/6J progenitor mice, and these strains were thus considered as susceptible to MAIDS. This bimodal strain distribution pattern of resistance/susceptibility to MAIDS among the RI strains suggests that this phenotype is controlled by a single gene. Linkage analysis with other allelic markers showed a strong association between resistance/susceptibility to MAIDS and the H-2 complex. Possession of the H-2b haplotype derived from C57BL/6J mice was associated with susceptibility to MAIDS, while the H-2a haplotype conferred resistance to the disease. This finding was confirmed by demonstrating that H-2a congenics on the susceptible C57BL/10 background were as resistant to MAIDS as A/J mice which donated the H-2a locus. Gene(s) within the H-2 complex thus represent the major regulatory mechanism of resistance/susceptibility to MAIDS."	Immunogenetics	1989		"Hamelin-Bourassa D, Skamene E, Gervais F."	2551819	8 - 12 weeks			weeks	>36		14 - 16			>42								23 - 26						>41				>28				>39		13 - 20		>41			>30	>41	18- 28 																	Nathan Copeland
Relationship between susceptibility/ resistance to MAIDS and the mouse MHC	H-2 haplotype	Susceptibility to a mouse acquired immunodeficiency syndrome is influenced by the H-2.	"The development of a mouse acquired immunodeficiency syndrome (MAIDS) induced following LP-BM5 MuLV infection depends on host genetic factors. Susceptible mice, such as C57BL/6J mice, develop a profound impairment of lymphoproliferative response to mitogens and hyperplasia of lymphoid organs and succumb to infection within 6 months. These changes do not occur in resistant mice, such as A/J mice. Resistance to MAIDS is a dominant trait since (C57BL/6J x A/J)F1 hybrid mice did not develop any immune dysfunctions following infection. Genetic regulation of the trait of resistance/susceptibility to MAIDS was determined in AXB/BXA recombinant inbred (RI) mouse strains (derived from resistant A/J and susceptible C57BL/6J progenitors). Two different criteria were used to determine their resistance or susceptibility to developing MAIDS: the gross pathologic evaluation of lymphoid organs at 13-15 weeks of infection, and survival. RI mouse strains segregated into two non-overlapping groups. The first group did not develop any significant pathology, and these mouse strains were considered as resistant to MAIDS. The second group showed the virus-induced pathological changes as well as an immunological dysfunction as seen in C57BL/6J progenitor mice, and these strains were thus considered as susceptible to MAIDS. This bimodal strain distribution pattern of resistance/susceptibility to MAIDS among the RI strains suggests that this phenotype is controlled by a single gene. Linkage analysis with other allelic markers showed a strong association between resistance/susceptibility to MAIDS and the H-2 complex. Possession of the H-2b haplotype derived from C57BL/6J mice was associated with susceptibility to MAIDS, while the H-2a haplotype conferred resistance to the disease. This finding was confirmed by demonstrating that H-2a congenics on the susceptible C57BL/10 background were as resistant to MAIDS as A/J mice which donated the H-2a locus. Gene(s) within the H-2 complex thus represent the major regulatory mechanism of resistance/susceptibility to MAIDS."	Immunogenetics	1989		"Hamelin-Bourassa D, Skamene E, Gervais F."	2551819	8 - 12 weeks				b		b			a								b						a	b	b		a				a		b		a			a	a	b			b						a			b					Nathan Copeland
% B6 response		Mapping lipopolysaccharide response loci in mice using recombinant inbred and congenic strains.	"Lipopolysaccharide (LPS) induces proliferation of splenic B-cells, and this response was found to be significantly lower in A/J than in C57BL/6J (B6) mice. Several strains and substrains mirrored the high and low responses of B6 and A/J. Assessment of 26 AXB/BXA recombinant inbred (RI) mouse strains identified 23 strains with a low (A/J-like), high (B6-like), or intermediate response. The three remaining RI strains exhibited a novel hyperresponsive phenotype significantly different from that of either founder strain. RI analysis identified four suggestive loci contributing to the LPS response, two of which were confirmed by analysis of congenic strains containing the donor genomic segment from a high- or low-responder strain on the opposite background. The combination of A/J and B6 alleles fixed to homozygosity at the four suggestive loci would occur in only 1 of 256 intercross progeny, but occurred several times among the RI strains."	Genomics	1999	Nov	"Matesic LE, De Maio A, Reeves RH."	10585765	8 - 9 weeks	male	8-Mar	%					104	72		141	98	148		74		85					78		668	449	156				103		159	17		37		83	-32			113	106	93	561			77							122	48	85	Nathan Copeland
AXB/BXA SDPs for 28 markers near suggestive loci	D1Mit380	Mapping lipopolysaccharide response loci in mice using recombinant inbred and congenic strains.	"Lipopolysaccharide (LPS) induces proliferation of splenic B-cells, and this response was found to be significantly lower in A/J than in C57BL/6J (B6) mice. Several strains and substrains mirrored the high and low responses of B6 and A/J. Assessment of 26 AXB/BXA recombinant inbred (RI) mouse strains identified 23 strains with a low (A/J-like), high (B6-like), or intermediate response. The three remaining RI strains exhibited a novel hyperresponsive phenotype significantly different from that of either founder strain. RI analysis identified four suggestive loci contributing to the LPS response, two of which were confirmed by analysis of congenic strains containing the donor genomic segment from a high- or low-responder strain on the opposite background. The combination of A/J and B6 alleles fixed to homozygosity at the four suggestive loci would occur in only 1 of 256 intercross progeny, but occurred several times among the RI strains."	Genomics	1999	Nov	"Matesic LE, De Maio A, Reeves RH."	10585765	8 - 9 weeks	male	8-Mar						B	A		A	A	B		A		A		A	A		B		B	B	B				A		A	B		A		A	A			A	A	A	B		B	A							B	B	A	Nathan Copeland
AXB/BXA SDPs for 28 markers near suggestive loci	D1Mit181	Mapping lipopolysaccharide response loci in mice using recombinant inbred and congenic strains.	"Lipopolysaccharide (LPS) induces proliferation of splenic B-cells, and this response was found to be significantly lower in A/J than in C57BL/6J (B6) mice. Several strains and substrains mirrored the high and low responses of B6 and A/J. Assessment of 26 AXB/BXA recombinant inbred (RI) mouse strains identified 23 strains with a low (A/J-like), high (B6-like), or intermediate response. The three remaining RI strains exhibited a novel hyperresponsive phenotype significantly different from that of either founder strain. RI analysis identified four suggestive loci contributing to the LPS response, two of which were confirmed by analysis of congenic strains containing the donor genomic segment from a high- or low-responder strain on the opposite background. The combination of A/J and B6 alleles fixed to homozygosity at the four suggestive loci would occur in only 1 of 256 intercross progeny, but occurred several times among the RI strains."	Genomics	1999	Nov	"Matesic LE, De Maio A, Reeves RH."	10585765	8 - 9 weeks	male	8-Mar						B	A		A	A	B		A		B		A	A		B		B	B	B				A		A	A		A		A	A			A	A	B	B		B	A							B	B	A	Nathan Copeland
AXB/BXA SDPs for 28 markers near suggestive loci	D1Mit437	Mapping lipopolysaccharide response loci in mice using recombinant inbred and congenic strains.	"Lipopolysaccharide (LPS) induces proliferation of splenic B-cells, and this response was found to be significantly lower in A/J than in C57BL/6J (B6) mice. Several strains and substrains mirrored the high and low responses of B6 and A/J. Assessment of 26 AXB/BXA recombinant inbred (RI) mouse strains identified 23 strains with a low (A/J-like), high (B6-like), or intermediate response. The three remaining RI strains exhibited a novel hyperresponsive phenotype significantly different from that of either founder strain. RI analysis identified four suggestive loci contributing to the LPS response, two of which were confirmed by analysis of congenic strains containing the donor genomic segment from a high- or low-responder strain on the opposite background. The combination of A/J and B6 alleles fixed to homozygosity at the four suggestive loci would occur in only 1 of 256 intercross progeny, but occurred several times among the RI strains."	Genomics	1999	Nov	"Matesic LE, De Maio A, Reeves RH."	10585765	8 - 9 weeks	male	8-Mar						B	A		A	A	B		A		A		A	A		B		B	B	B				A		A	A		A		A	A			A	A	A	B		B	A							B	A	A	Nathan Copeland
AXB/BXA SDPs for 28 markers near suggestive loci	D7Mit340	Mapping lipopolysaccharide response loci in mice using recombinant inbred and congenic strains.	"Lipopolysaccharide (LPS) induces proliferation of splenic B-cells, and this response was found to be significantly lower in A/J than in C57BL/6J (B6) mice. Several strains and substrains mirrored the high and low responses of B6 and A/J. Assessment of 26 AXB/BXA recombinant inbred (RI) mouse strains identified 23 strains with a low (A/J-like), high (B6-like), or intermediate response. The three remaining RI strains exhibited a novel hyperresponsive phenotype significantly different from that of either founder strain. RI analysis identified four suggestive loci contributing to the LPS response, two of which were confirmed by analysis of congenic strains containing the donor genomic segment from a high- or low-responder strain on the opposite background. The combination of A/J and B6 alleles fixed to homozygosity at the four suggestive loci would occur in only 1 of 256 intercross progeny, but occurred several times among the RI strains."	Genomics	1999	Nov	"Matesic LE, De Maio A, Reeves RH."	10585765	8 - 9 weeks	male	8-Mar						B	B		A	A	A		B		B		B	A		A		A	A	A				B		A	B		B		A	A			B	A	A	A		B	A							B	A	A	Nathan Copeland
AXB/BXA SDPs for 28 markers near suggestive loci	D7Mit117	Mapping lipopolysaccharide response loci in mice using recombinant inbred and congenic strains.	"Lipopolysaccharide (LPS) induces proliferation of splenic B-cells, and this response was found to be significantly lower in A/J than in C57BL/6J (B6) mice. Several strains and substrains mirrored the high and low responses of B6 and A/J. Assessment of 26 AXB/BXA recombinant inbred (RI) mouse strains identified 23 strains with a low (A/J-like), high (B6-like), or intermediate response. The three remaining RI strains exhibited a novel hyperresponsive phenotype significantly different from that of either founder strain. RI analysis identified four suggestive loci contributing to the LPS response, two of which were confirmed by analysis of congenic strains containing the donor genomic segment from a high- or low-responder strain on the opposite background. The combination of A/J and B6 alleles fixed to homozygosity at the four suggestive loci would occur in only 1 of 256 intercross progeny, but occurred several times among the RI strains."	Genomics	1999	Nov	"Matesic LE, De Maio A, Reeves RH."	10585765	8 - 9 weeks	male	8-Mar						B	A		A	A	A		B		B		A	A		A		A	A	A				B		B	B		A		A	A			A	A	A	A		B	A							A	A	A	Nathan Copeland
AXB/BXA SDPs for 28 markers near suggestive loci	D7Mit155	Mapping lipopolysaccharide response loci in mice using recombinant inbred and congenic strains.	"Lipopolysaccharide (LPS) induces proliferation of splenic B-cells, and this response was found to be significantly lower in A/J than in C57BL/6J (B6) mice. Several strains and substrains mirrored the high and low responses of B6 and A/J. Assessment of 26 AXB/BXA recombinant inbred (RI) mouse strains identified 23 strains with a low (A/J-like), high (B6-like), or intermediate response. The three remaining RI strains exhibited a novel hyperresponsive phenotype significantly different from that of either founder strain. RI analysis identified four suggestive loci contributing to the LPS response, two of which were confirmed by analysis of congenic strains containing the donor genomic segment from a high- or low-responder strain on the opposite background. The combination of A/J and B6 alleles fixed to homozygosity at the four suggestive loci would occur in only 1 of 256 intercross progeny, but occurred several times among the RI strains."	Genomics	1999	Nov	"Matesic LE, De Maio A, Reeves RH."	10585765	8 - 9 weeks	male	8-Mar						B	A		B	A	A		B		B		A	A		A		B	B	B				B		B	A		A		A	A			A	A	A	B		B	A							A	A	A	Nathan Copeland
AXB/BXA SDPs for 28 markers near suggestive loci	D7Mit309	Mapping lipopolysaccharide response loci in mice using recombinant inbred and congenic strains.	"Lipopolysaccharide (LPS) induces proliferation of splenic B-cells, and this response was found to be significantly lower in A/J than in C57BL/6J (B6) mice. Several strains and substrains mirrored the high and low responses of B6 and A/J. Assessment of 26 AXB/BXA recombinant inbred (RI) mouse strains identified 23 strains with a low (A/J-like), high (B6-like), or intermediate response. The three remaining RI strains exhibited a novel hyperresponsive phenotype significantly different from that of either founder strain. RI analysis identified four suggestive loci contributing to the LPS response, two of which were confirmed by analysis of congenic strains containing the donor genomic segment from a high- or low-responder strain on the opposite background. The combination of A/J and B6 alleles fixed to homozygosity at the four suggestive loci would occur in only 1 of 256 intercross progeny, but occurred several times among the RI strains."	Genomics	1999	Nov	"Matesic LE, De Maio A, Reeves RH."	10585765	8 - 9 weeks	male	8-Mar						B	B			A	A		B		B		A	A		A		B	B	B				B		B	A		A		B	A			A	A	A	B		B	A							A	A	A	Nathan Copeland
AXB/BXA SDPs for 28 markers near suggestive loci	D7Mit301	Mapping lipopolysaccharide response loci in mice using recombinant inbred and congenic strains.	"Lipopolysaccharide (LPS) induces proliferation of splenic B-cells, and this response was found to be significantly lower in A/J than in C57BL/6J (B6) mice. Several strains and substrains mirrored the high and low responses of B6 and A/J. Assessment of 26 AXB/BXA recombinant inbred (RI) mouse strains identified 23 strains with a low (A/J-like), high (B6-like), or intermediate response. The three remaining RI strains exhibited a novel hyperresponsive phenotype significantly different from that of either founder strain. RI analysis identified four suggestive loci contributing to the LPS response, two of which were confirmed by analysis of congenic strains containing the donor genomic segment from a high- or low-responder strain on the opposite background. The combination of A/J and B6 alleles fixed to homozygosity at the four suggestive loci would occur in only 1 of 256 intercross progeny, but occurred several times among the RI strains."	Genomics	1999	Nov	"Matesic LE, De Maio A, Reeves RH."	10585765	8 - 9 weeks	male	8-Mar						B	A		B	A	A		B		B		A	A		B		B	B	B				B		B	A		A		A	B			B	B	A	A		A	B							A	B	A	Nathan Copeland
AXB/BXA SDPs for 28 markers near suggestive loci	D7Mit281	Mapping lipopolysaccharide response loci in mice using recombinant inbred and congenic strains.	"Lipopolysaccharide (LPS) induces proliferation of splenic B-cells, and this response was found to be significantly lower in A/J than in C57BL/6J (B6) mice. Several strains and substrains mirrored the high and low responses of B6 and A/J. Assessment of 26 AXB/BXA recombinant inbred (RI) mouse strains identified 23 strains with a low (A/J-like), high (B6-like), or intermediate response. The three remaining RI strains exhibited a novel hyperresponsive phenotype significantly different from that of either founder strain. RI analysis identified four suggestive loci contributing to the LPS response, two of which were confirmed by analysis of congenic strains containing the donor genomic segment from a high- or low-responder strain on the opposite background. The combination of A/J and B6 alleles fixed to homozygosity at the four suggestive loci would occur in only 1 of 256 intercross progeny, but occurred several times among the RI strains."	Genomics	1999	Nov	"Matesic LE, De Maio A, Reeves RH."	10585765	8 - 9 weeks	male	8-Mar						B	A		B	A	A		B		B		A	A		B		B	B	B				B		A	B		A		A	B			B	B	A	A		B	B							B	B	A	Nathan Copeland
AXB/BXA SDPs for 28 markers near suggestive loci	D7Mit238	Mapping lipopolysaccharide response loci in mice using recombinant inbred and congenic strains.	"Lipopolysaccharide (LPS) induces proliferation of splenic B-cells, and this response was found to be significantly lower in A/J than in C57BL/6J (B6) mice. Several strains and substrains mirrored the high and low responses of B6 and A/J. Assessment of 26 AXB/BXA recombinant inbred (RI) mouse strains identified 23 strains with a low (A/J-like), high (B6-like), or intermediate response. The three remaining RI strains exhibited a novel hyperresponsive phenotype significantly different from that of either founder strain. RI analysis identified four suggestive loci contributing to the LPS response, two of which were confirmed by analysis of congenic strains containing the donor genomic segment from a high- or low-responder strain on the opposite background. The combination of A/J and B6 alleles fixed to homozygosity at the four suggestive loci would occur in only 1 of 256 intercross progeny, but occurred several times among the RI strains."	Genomics	1999	Nov	"Matesic LE, De Maio A, Reeves RH."	10585765	8 - 9 weeks	male	8-Mar						B	A		B	A	A		B		B		A	A		B		B	B	B				B		B	B		A		A	B			B	B	A	A		A	B							B	B	A	Nathan Copeland
AXB/BXA SDPs for 28 markers near suggestive loci	D7Mit285	Mapping lipopolysaccharide response loci in mice using recombinant inbred and congenic strains.	"Lipopolysaccharide (LPS) induces proliferation of splenic B-cells, and this response was found to be significantly lower in A/J than in C57BL/6J (B6) mice. Several strains and substrains mirrored the high and low responses of B6 and A/J. Assessment of 26 AXB/BXA recombinant inbred (RI) mouse strains identified 23 strains with a low (A/J-like), high (B6-like), or intermediate response. The three remaining RI strains exhibited a novel hyperresponsive phenotype significantly different from that of either founder strain. RI analysis identified four suggestive loci contributing to the LPS response, two of which were confirmed by analysis of congenic strains containing the donor genomic segment from a high- or low-responder strain on the opposite background. The combination of A/J and B6 alleles fixed to homozygosity at the four suggestive loci would occur in only 1 of 256 intercross progeny, but occurred several times among the RI strains."	Genomics	1999	Nov	"Matesic LE, De Maio A, Reeves RH."	10585765	8 - 9 weeks	male	8-Mar						A	A		B	A	A		A		B		A	A		B		B	B	B				B		B	B		A		B	B			B	B	A	A		A	B							B	B	A	Nathan Copeland
AXB/BXA SDPs for 28 markers near suggestive loci	D7Mit187	Mapping lipopolysaccharide response loci in mice using recombinant inbred and congenic strains.	"Lipopolysaccharide (LPS) induces proliferation of splenic B-cells, and this response was found to be significantly lower in A/J than in C57BL/6J (B6) mice. Several strains and substrains mirrored the high and low responses of B6 and A/J. Assessment of 26 AXB/BXA recombinant inbred (RI) mouse strains identified 23 strains with a low (A/J-like), high (B6-like), or intermediate response. The three remaining RI strains exhibited a novel hyperresponsive phenotype significantly different from that of either founder strain. RI analysis identified four suggestive loci contributing to the LPS response, two of which were confirmed by analysis of congenic strains containing the donor genomic segment from a high- or low-responder strain on the opposite background. The combination of A/J and B6 alleles fixed to homozygosity at the four suggestive loci would occur in only 1 of 256 intercross progeny, but occurred several times among the RI strains."	Genomics	1999	Nov	"Matesic LE, De Maio A, Reeves RH."	10585765	8 - 9 weeks	male	8-Mar						A	B		B	B	A		A		B		A	A		A		B	B	B				B		B	B		A		B	A			B	B	A	A		A	A							B	B	A	Nathan Copeland
AXB/BXA SDPs for 28 markers near suggestive loci	D9Mit352	Mapping lipopolysaccharide response loci in mice using recombinant inbred and congenic strains.	"Lipopolysaccharide (LPS) induces proliferation of splenic B-cells, and this response was found to be significantly lower in A/J than in C57BL/6J (B6) mice. Several strains and substrains mirrored the high and low responses of B6 and A/J. Assessment of 26 AXB/BXA recombinant inbred (RI) mouse strains identified 23 strains with a low (A/J-like), high (B6-like), or intermediate response. The three remaining RI strains exhibited a novel hyperresponsive phenotype significantly different from that of either founder strain. RI analysis identified four suggestive loci contributing to the LPS response, two of which were confirmed by analysis of congenic strains containing the donor genomic segment from a high- or low-responder strain on the opposite background. The combination of A/J and B6 alleles fixed to homozygosity at the four suggestive loci would occur in only 1 of 256 intercross progeny, but occurred several times among the RI strains."	Genomics	1999	Nov	"Matesic LE, De Maio A, Reeves RH."	10585765	8 - 9 weeks	male	8-Mar						A	A		B		B		A				B	B		A		A	A	A						A	A		B		A	A			B	A	A	B		A	A							A	B	B	Nathan Copeland
AXB/BXA SDPs for 28 markers near suggestive loci1	D11Mit208	Mapping lipopolysaccharide response loci in mice using recombinant inbred and congenic strains.	"Lipopolysaccharide (LPS) induces proliferation of splenic B-cells, and this response was found to be significantly lower in A/J than in C57BL/6J (B6) mice. Several strains and substrains mirrored the high and low responses of B6 and A/J. Assessment of 26 AXB/BXA recombinant inbred (RI) mouse strains identified 23 strains with a low (A/J-like), high (B6-like), or intermediate response. The three remaining RI strains exhibited a novel hyperresponsive phenotype significantly different from that of either founder strain. RI analysis identified four suggestive loci contributing to the LPS response, two of which were confirmed by analysis of congenic strains containing the donor genomic segment from a high- or low-responder strain on the opposite background. The combination of A/J and B6 alleles fixed to homozygosity at the four suggestive loci would occur in only 1 of 256 intercross progeny, but occurred several times among the RI strains."	Genomics	1999	Nov	"Matesic LE, De Maio A, Reeves RH."	10585765	8 - 9 weeks	male	8-Mar						B	B		B	A	A		A		B		A	B		A		A	A	A				A		A	B		B		A	B			B	B	B	A		A	B							A	B	B	Nathan Copeland
AXB/BXA SDPs for 28 markers near suggestive loci1	D11Mit298	Mapping lipopolysaccharide response loci in mice using recombinant inbred and congenic strains.	"Lipopolysaccharide (LPS) induces proliferation of splenic B-cells, and this response was found to be significantly lower in A/J than in C57BL/6J (B6) mice. Several strains and substrains mirrored the high and low responses of B6 and A/J. Assessment of 26 AXB/BXA recombinant inbred (RI) mouse strains identified 23 strains with a low (A/J-like), high (B6-like), or intermediate response. The three remaining RI strains exhibited a novel hyperresponsive phenotype significantly different from that of either founder strain. RI analysis identified four suggestive loci contributing to the LPS response, two of which were confirmed by analysis of congenic strains containing the donor genomic segment from a high- or low-responder strain on the opposite background. The combination of A/J and B6 alleles fixed to homozygosity at the four suggestive loci would occur in only 1 of 256 intercross progeny, but occurred several times among the RI strains."	Genomics	1999	Nov	"Matesic LE, De Maio A, Reeves RH."	10585765	8 - 9 weeks	male	8-Mar						B	B		B	B	A		A		B		A	B		A		A	A	A				A		A	B		B		A	B			B	A	B	A		A	B							A	B	B	Nathan Copeland
AXB/BXA SDPs for 28 markers near suggestive loci1	D11Mit321	Mapping lipopolysaccharide response loci in mice using recombinant inbred and congenic strains.	"Lipopolysaccharide (LPS) induces proliferation of splenic B-cells, and this response was found to be significantly lower in A/J than in C57BL/6J (B6) mice. Several strains and substrains mirrored the high and low responses of B6 and A/J. Assessment of 26 AXB/BXA recombinant inbred (RI) mouse strains identified 23 strains with a low (A/J-like), high (B6-like), or intermediate response. The three remaining RI strains exhibited a novel hyperresponsive phenotype significantly different from that of either founder strain. RI analysis identified four suggestive loci contributing to the LPS response, two of which were confirmed by analysis of congenic strains containing the donor genomic segment from a high- or low-responder strain on the opposite background. The combination of A/J and B6 alleles fixed to homozygosity at the four suggestive loci would occur in only 1 of 256 intercross progeny, but occurred several times among the RI strains."	Genomics	1999	Nov	"Matesic LE, De Maio A, Reeves RH."	10585765	8 - 9 weeks	male	8-Mar						B	B		B	B	B		A		B		B	B		A		A	A	A				A		A	B		B		A	B			A	A	B	A		A	B							A	B	B	Nathan Copeland
AXB/BXA SDPs for 28 markers near suggestive loci1	D12Mit8	Mapping lipopolysaccharide response loci in mice using recombinant inbred and congenic strains.	"Lipopolysaccharide (LPS) induces proliferation of splenic B-cells, and this response was found to be significantly lower in A/J than in C57BL/6J (B6) mice. Several strains and substrains mirrored the high and low responses of B6 and A/J. Assessment of 26 AXB/BXA recombinant inbred (RI) mouse strains identified 23 strains with a low (A/J-like), high (B6-like), or intermediate response. The three remaining RI strains exhibited a novel hyperresponsive phenotype significantly different from that of either founder strain. RI analysis identified four suggestive loci contributing to the LPS response, two of which were confirmed by analysis of congenic strains containing the donor genomic segment from a high- or low-responder strain on the opposite background. The combination of A/J and B6 alleles fixed to homozygosity at the four suggestive loci would occur in only 1 of 256 intercross progeny, but occurred several times among the RI strains."	Genomics	1999	Nov	"Matesic LE, De Maio A, Reeves RH."	10585765	8 - 9 weeks	male	8-Mar						A	A		A	A	B		B		B		B	B		A		B	B	B				B		B	B				B	A			A	A	B	A		A	A							A	A	A	Nathan Copeland
AXB/BXA SDPs for 28 markers near suggestive loci1	D13Mit17	Mapping lipopolysaccharide response loci in mice using recombinant inbred and congenic strains.	"Lipopolysaccharide (LPS) induces proliferation of splenic B-cells, and this response was found to be significantly lower in A/J than in C57BL/6J (B6) mice. Several strains and substrains mirrored the high and low responses of B6 and A/J. Assessment of 26 AXB/BXA recombinant inbred (RI) mouse strains identified 23 strains with a low (A/J-like), high (B6-like), or intermediate response. The three remaining RI strains exhibited a novel hyperresponsive phenotype significantly different from that of either founder strain. RI analysis identified four suggestive loci contributing to the LPS response, two of which were confirmed by analysis of congenic strains containing the donor genomic segment from a high- or low-responder strain on the opposite background. The combination of A/J and B6 alleles fixed to homozygosity at the four suggestive loci would occur in only 1 of 256 intercross progeny, but occurred several times among the RI strains."	Genomics	1999	Nov	"Matesic LE, De Maio A, Reeves RH."	10585765	8 - 9 weeks	male	8-Mar						A	A		A	B	B		B		A		B	B		A		A	A	A				B		A	A		A		B	A			B	A	B	A		B	A							B	B	B	Nathan Copeland
AXB/BXA SDPs for 28 markers near suggestive loci1	D13Mit254	Mapping lipopolysaccharide response loci in mice using recombinant inbred and congenic strains.	"Lipopolysaccharide (LPS) induces proliferation of splenic B-cells, and this response was found to be significantly lower in A/J than in C57BL/6J (B6) mice. Several strains and substrains mirrored the high and low responses of B6 and A/J. Assessment of 26 AXB/BXA recombinant inbred (RI) mouse strains identified 23 strains with a low (A/J-like), high (B6-like), or intermediate response. The three remaining RI strains exhibited a novel hyperresponsive phenotype significantly different from that of either founder strain. RI analysis identified four suggestive loci contributing to the LPS response, two of which were confirmed by analysis of congenic strains containing the donor genomic segment from a high- or low-responder strain on the opposite background. The combination of A/J and B6 alleles fixed to homozygosity at the four suggestive loci would occur in only 1 of 256 intercross progeny, but occurred several times among the RI strains."	Genomics	1999	Nov	"Matesic LE, De Maio A, Reeves RH."	10585765	8 - 9 weeks	male	8-Mar						A	B		A	A	A		A		B		B	A		A		A	A	A				B		B	B		B		B	B			B	A	B	B		A	B							B	B	B	Nathan Copeland
AXB/BXA SDPs for 28 markers near suggestive loci1	D13Mit126	Mapping lipopolysaccharide response loci in mice using recombinant inbred and congenic strains.	"Lipopolysaccharide (LPS) induces proliferation of splenic B-cells, and this response was found to be significantly lower in A/J than in C57BL/6J (B6) mice. Several strains and substrains mirrored the high and low responses of B6 and A/J. Assessment of 26 AXB/BXA recombinant inbred (RI) mouse strains identified 23 strains with a low (A/J-like), high (B6-like), or intermediate response. The three remaining RI strains exhibited a novel hyperresponsive phenotype significantly different from that of either founder strain. RI analysis identified four suggestive loci contributing to the LPS response, two of which were confirmed by analysis of congenic strains containing the donor genomic segment from a high- or low-responder strain on the opposite background. The combination of A/J and B6 alleles fixed to homozygosity at the four suggestive loci would occur in only 1 of 256 intercross progeny, but occurred several times among the RI strains."	Genomics	1999	Nov	"Matesic LE, De Maio A, Reeves RH."	10585765	8 - 9 weeks	male	8-Mar						A	B		A	A	A		B		B		B	A		A		A	A	A				B		B	B		B		B	B			B	A	B	A		A	B							B	B	B	Nathan Copeland
AXB/BXA SDPs for 28 markers near suggestive loci1	D13Mit106	Mapping lipopolysaccharide response loci in mice using recombinant inbred and congenic strains.	"Lipopolysaccharide (LPS) induces proliferation of splenic B-cells, and this response was found to be significantly lower in A/J than in C57BL/6J (B6) mice. Several strains and substrains mirrored the high and low responses of B6 and A/J. Assessment of 26 AXB/BXA recombinant inbred (RI) mouse strains identified 23 strains with a low (A/J-like), high (B6-like), or intermediate response. The three remaining RI strains exhibited a novel hyperresponsive phenotype significantly different from that of either founder strain. RI analysis identified four suggestive loci contributing to the LPS response, two of which were confirmed by analysis of congenic strains containing the donor genomic segment from a high- or low-responder strain on the opposite background. The combination of A/J and B6 alleles fixed to homozygosity at the four suggestive loci would occur in only 1 of 256 intercross progeny, but occurred several times among the RI strains."	Genomics	1999	Nov	"Matesic LE, De Maio A, Reeves RH."	10585765	8 - 9 weeks	male	8-Mar						A	A		A	B	A		B		B		B	A		A		A	A	A				B		B	B		B		B	B			B	A	B	A		A	B							B	B	B	Nathan Copeland
AXB/BXA SDPs for 28 markers near suggestive loci1	D13Mit287	Mapping lipopolysaccharide response loci in mice using recombinant inbred and congenic strains.	"Lipopolysaccharide (LPS) induces proliferation of splenic B-cells, and this response was found to be significantly lower in A/J than in C57BL/6J (B6) mice. Several strains and substrains mirrored the high and low responses of B6 and A/J. Assessment of 26 AXB/BXA recombinant inbred (RI) mouse strains identified 23 strains with a low (A/J-like), high (B6-like), or intermediate response. The three remaining RI strains exhibited a novel hyperresponsive phenotype significantly different from that of either founder strain. RI analysis identified four suggestive loci contributing to the LPS response, two of which were confirmed by analysis of congenic strains containing the donor genomic segment from a high- or low-responder strain on the opposite background. The combination of A/J and B6 alleles fixed to homozygosity at the four suggestive loci would occur in only 1 of 256 intercross progeny, but occurred several times among the RI strains."	Genomics	1999	Nov	"Matesic LE, De Maio A, Reeves RH."	10585765	8 - 9 weeks	male	8-Mar						A	A		A	A	B		A		B		A	A		A		A	A	A				B		B	B		B		A	B			B	B	B	A		A	B							B	B	B	Nathan Copeland
AXB/BXA SDPs for 28 markers near suggestive loci1	D13Mit213	Mapping lipopolysaccharide response loci in mice using recombinant inbred and congenic strains.	"Lipopolysaccharide (LPS) induces proliferation of splenic B-cells, and this response was found to be significantly lower in A/J than in C57BL/6J (B6) mice. Several strains and substrains mirrored the high and low responses of B6 and A/J. Assessment of 26 AXB/BXA recombinant inbred (RI) mouse strains identified 23 strains with a low (A/J-like), high (B6-like), or intermediate response. The three remaining RI strains exhibited a novel hyperresponsive phenotype significantly different from that of either founder strain. RI analysis identified four suggestive loci contributing to the LPS response, two of which were confirmed by analysis of congenic strains containing the donor genomic segment from a high- or low-responder strain on the opposite background. The combination of A/J and B6 alleles fixed to homozygosity at the four suggestive loci would occur in only 1 of 256 intercross progeny, but occurred several times among the RI strains."	Genomics	1999	Nov	"Matesic LE, De Maio A, Reeves RH."	10585765	8 - 9 weeks	male	8-Mar						A	A		A	B	A		B		B		A	B		A		A	A	A				A		B	B		B		A	B			B	B	B	A		A	B							A	B	B	Nathan Copeland
AXB/BXA SDPs for 28 markers near suggestive loci1	Tnf	Mapping lipopolysaccharide response loci in mice using recombinant inbred and congenic strains.	"Lipopolysaccharide (LPS) induces proliferation of splenic B-cells, and this response was found to be significantly lower in A/J than in C57BL/6J (B6) mice. Several strains and substrains mirrored the high and low responses of B6 and A/J. Assessment of 26 AXB/BXA recombinant inbred (RI) mouse strains identified 23 strains with a low (A/J-like), high (B6-like), or intermediate response. The three remaining RI strains exhibited a novel hyperresponsive phenotype significantly different from that of either founder strain. RI analysis identified four suggestive loci contributing to the LPS response, two of which were confirmed by analysis of congenic strains containing the donor genomic segment from a high- or low-responder strain on the opposite background. The combination of A/J and B6 alleles fixed to homozygosity at the four suggestive loci would occur in only 1 of 256 intercross progeny, but occurred several times among the RI strains."	Genomics	1999	Nov	"Matesic LE, De Maio A, Reeves RH."	10585765	8 - 9 weeks	male	8-Mar						A	A		B	A	B		A		B		A	B		A		B	B	B				A		B	B		A		B	A			B	A	B	B		B	A							B	A	A	Nathan Copeland
AXB/BXA SDPs for 28 markers near suggestive loci1	D17Mit176	Mapping lipopolysaccharide response loci in mice using recombinant inbred and congenic strains.	"Lipopolysaccharide (LPS) induces proliferation of splenic B-cells, and this response was found to be significantly lower in A/J than in C57BL/6J (B6) mice. Several strains and substrains mirrored the high and low responses of B6 and A/J. Assessment of 26 AXB/BXA recombinant inbred (RI) mouse strains identified 23 strains with a low (A/J-like), high (B6-like), or intermediate response. The three remaining RI strains exhibited a novel hyperresponsive phenotype significantly different from that of either founder strain. RI analysis identified four suggestive loci contributing to the LPS response, two of which were confirmed by analysis of congenic strains containing the donor genomic segment from a high- or low-responder strain on the opposite background. The combination of A/J and B6 alleles fixed to homozygosity at the four suggestive loci would occur in only 1 of 256 intercross progeny, but occurred several times among the RI strains."	Genomics	1999	Nov	"Matesic LE, De Maio A, Reeves RH."	10585765	8 - 9 weeks	male	8-Mar						A	A		B	A	B		A		B		B	B		B		B	B	B				A		B	B		A		B	B			B	A	B	B		B	B							B	A	B	Nathan Copeland
AXB/BXA SDPs for 28 markers near suggestive loci1	D17Mit66	Mapping lipopolysaccharide response loci in mice using recombinant inbred and congenic strains.	"Lipopolysaccharide (LPS) induces proliferation of splenic B-cells, and this response was found to be significantly lower in A/J than in C57BL/6J (B6) mice. Several strains and substrains mirrored the high and low responses of B6 and A/J. Assessment of 26 AXB/BXA recombinant inbred (RI) mouse strains identified 23 strains with a low (A/J-like), high (B6-like), or intermediate response. The three remaining RI strains exhibited a novel hyperresponsive phenotype significantly different from that of either founder strain. RI analysis identified four suggestive loci contributing to the LPS response, two of which were confirmed by analysis of congenic strains containing the donor genomic segment from a high- or low-responder strain on the opposite background. The combination of A/J and B6 alleles fixed to homozygosity at the four suggestive loci would occur in only 1 of 256 intercross progeny, but occurred several times among the RI strains."	Genomics	1999	Nov	"Matesic LE, De Maio A, Reeves RH."	10585765	8 - 9 weeks	male	8-Mar						A	A		B	A	B		A		B		B	B		B		B	B	B				A		B	B		A		B	B			B	A	A	B		B	B							B	A	B	Nathan Copeland
AXB/BXA SDPs for 28 markers near suggestive loci1	D17Mit139	Mapping lipopolysaccharide response loci in mice using recombinant inbred and congenic strains.	"Lipopolysaccharide (LPS) induces proliferation of splenic B-cells, and this response was found to be significantly lower in A/J than in C57BL/6J (B6) mice. Several strains and substrains mirrored the high and low responses of B6 and A/J. Assessment of 26 AXB/BXA recombinant inbred (RI) mouse strains identified 23 strains with a low (A/J-like), high (B6-like), or intermediate response. The three remaining RI strains exhibited a novel hyperresponsive phenotype significantly different from that of either founder strain. RI analysis identified four suggestive loci contributing to the LPS response, two of which were confirmed by analysis of congenic strains containing the donor genomic segment from a high- or low-responder strain on the opposite background. The combination of A/J and B6 alleles fixed to homozygosity at the four suggestive loci would occur in only 1 of 256 intercross progeny, but occurred several times among the RI strains."	Genomics	1999	Nov	"Matesic LE, De Maio A, Reeves RH."	10585765	8 - 9 weeks	male	8-Mar						A	A		B	A	A		A		B		A	B		A		B	B	B				A		B	B		A		B	B			B	A	A	B		B	B							B	A	B	Nathan Copeland
AXB/BXA SDPs for 28 markers near suggestive loci1	D17Mit159	Mapping lipopolysaccharide response loci in mice using recombinant inbred and congenic strains.	"Lipopolysaccharide (LPS) induces proliferation of splenic B-cells, and this response was found to be significantly lower in A/J than in C57BL/6J (B6) mice. Several strains and substrains mirrored the high and low responses of B6 and A/J. Assessment of 26 AXB/BXA recombinant inbred (RI) mouse strains identified 23 strains with a low (A/J-like), high (B6-like), or intermediate response. The three remaining RI strains exhibited a novel hyperresponsive phenotype significantly different from that of either founder strain. RI analysis identified four suggestive loci contributing to the LPS response, two of which were confirmed by analysis of congenic strains containing the donor genomic segment from a high- or low-responder strain on the opposite background. The combination of A/J and B6 alleles fixed to homozygosity at the four suggestive loci would occur in only 1 of 256 intercross progeny, but occurred several times among the RI strains."	Genomics	1999	Nov	"Matesic LE, De Maio A, Reeves RH."	10585765	8 - 9 weeks	male	8-Mar						B	B		B	B	B		A		B		B	B		B		B	B	B				A		B	B		B		B	A			A	A	A	B		B	A							B	B	B	Nathan Copeland