This site provides access to raw data from various QTL (quantitative trait loci) studies using rodent inbred line crosses. Most data are available in the .csv fromat used by R/qtl and pseudomarker programs. In some cases analysis scripts and/or results are posted to accompany the data.
These data are provided as a courtesy to the genetic mapping community and may be used for purposes of developing or testing new analysis methods or software and for meta-analysis of quantitative traits. The authors of the datasets retain individual ownership of the data. We request, as a courtesy to the authors, that you alert them in advance of any publications that result from reanalysis of these data or obtain permission prior to redistribution of data or results.
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Ron Korstanje, John J. Albers, Gertrud Wolfbauer, Renhua Li, An-Yue Tu, Gary A.Churchill and Beverly J. Paigen:
Quantitative trait locus mapping of genes that regulate phospholipid transfer activity in SM/J and NZB/BlNJ inbred mice
Published in: Arteriosclerosis, Thrombosis, and Vascular Biology ( Arterioscler. Thromb. Vasc. Biol. 2004;24;155-160; originally published online Oct 30, 2003;DOI: 10.1161/01.ATV.0000104241.44819.10)
Data Downloads:
pltp.csv
Objective: Phospholipid transfer protein (PLTP), an important protein in the transfer of phospholipids between lipoprotein
particles and in the remodeling of HDL, is regulated at both the transcriptional and the protein level. We performed
quantitative trait locus (QTL) analysis to identify genomic loci regulating PLTP activity in mice.
Methods and Results: Plasma PLTP activity was measured in 217 male F2 progeny from a SM/J X NZB/B1NJ intercross.
Two QTL for plasma PLTP activity in mice fed chow (Pltpq1 and Pltpq2) were found on chromosomes 3 (34 cM,
logarithm of odds [LOD] 3.5) and 10 (66 cM, LOD 4.1); two additional QTL in mice fed atherogenic diet (Pltpq3 and
Pltpq4) were found on chromosomes 9 (56 cM, LOD 4.5) and 15 (34 cM, LOD 5.0); and one QTL (Pltiq1) for the
inducibility of PLTP activity was found on chromosome 4 (70 cM, LOD 3.7). Several candidate genes for these 5 QTL
were tested by sequence comparison and expression studies.
Conclusions: We identified five significant loci involved in PLTP activity in the mouse and provided supporting evidence
for the candidacy of Nr1h4 and Apof as the genes underlying Pltpq2. (Arterioscler Thromb Vasc Biol. 2004;
24:155-160.)
Naoki Ishimori, Renhua Li, Peter M. Kelmenson, Ron Korstanje, Kenneth A. Walsh, Gary A. Churchill, Kristina Forsman-Semb and Beverly Paigen:
Quantitative Trait Loci Analysis for Plasma HDL-Cholesterol Concentrations and Atherosclerosis Susceptibility Between Inbred Mouse Strains C57BL/6J and 129S1/SvImJ.
Published in: Arterioscler. Thromb. Vasc. Biol. 2004;24;161-166; originally published online Oct 30, 2003; DOI: 10.1161/01.ATV.0000104027.52895.D7
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Abstract :
Objective: The C57BL/6 (B6) and 129 mouse inbred strains differ markedly in plasma HDL-cholesterol concentrations and atherosclerosis susceptibility after a high-fat diet consumption. To identify loci controlling these traits, we performed quantitative trait loci (QTL) analysis.
Methods and Results: We fed a high-fat diet to 294 (B6x129S1/SvImJ)F2 females for 14 weeks, measured plasma HDL concentrations and size of aortic fatty-streak lesions, genotyped F2 females, and performed QTL analysis. HDL oncentrations were affected by six loci: Hdlq14 and Hdlq15 on chromosome 1 (peaks cM 80 and cM 104, logarithm of odds [LOD] 5.3 and 9.7, respectively); Hdlq16 on chromosome 8 (cM 44, LOD 2.6); Hdlq17 on chromosome 9 (cM 24, LOD 2.9); Hdlq18 on chromosome 12 (cM 20, LOD 5.9); and Hdlq19 on chromosome 2 (cM 90), which interacted with Hdlq15. Atherosclerosis susceptibility was affected by five loci: Ath17 on chromosome 10 (cM 34, LOD 6.6); Ath18 on chromosome 12 (cM 16, LOD 3.7); Ath19 (chromosome 11, cM 60), which interacted with Ath18; and Ath20 (chromosome 10, cM 10), which interacted with Ath21 (chromosome 12, cM 50).
Conclusions: We identified six loci for HDL and five loci for atherosclerosis susceptibility in a (B6x129S1/SvImJ)F2 intercross.
Luanne L. Peters, Rebecca A. Swearingen, Sabra G. Andersen, Babette Gwynn, Amy J. Lambert, Renhua Li, Samuel E. Lux, and Gary A. Churchill
Published in: The American Society of Hematology, 2004
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Abstract :
+/wan and CAST/Ei+/+ F1 hybrids. Hematologic and survival data from C3H, CAST/Ei F2 wan homozygotes support the hypothesis that genetic modifiers significantly influence the band-3 null HS phenotype. Significant QTL were identified for the MCV trait only, suggesting that RBC membrane characteristics are a target for modifier gene action. The most significant quantitative trait locus, Hsm1 (hereditary spherocytosis modifier 1), localizes to mouse Chromosome 12 and is dominant. The peak LOD score was obtained with a marker for Spnb1 encoding erythroid ß-spectrin, an obvious candidate gene. (Blood. 2004;103: 3233-3240)
Henning Wittenburg, Malcolm A. Lyons, Renhua Li, Gary A. Churchill, Martin C. Carey and Beverly Paigen: Published in: the American Gastroenterological Association 2003 (GASTROENTEROLOGY 2003;125:868–881 doi:10.1016/S0016-5085(03)01053-9) Data Downloads:
Abstract : Aims and Background: Cholesterol gallstone formation is a complex genetic trait. To identify additional cholesterol gallstone susceptibility loci, we performed a quantitative trait locus analysis using an intercross of PERA/Ei and I/LnJ inbred strains of mice. Methods: Mice of both sexes were examined for gallstone weight and evaluated according to a scoring system for the physical chemistry of cholelithiasis during feeding of a lithogenic diet. Intercross offspring were genotyped, and linkage analysis was performed by interval mapping. Differences in messenger RNA expression of positional candidate genes were determined using reverse-transcription and real-time polymerase chain reaction. Results: We identified significant loci associated with gallstone weight on chromosomes 10 and 4, named Lith7 and Lith8, respectively (both susceptibility alleles conferred by strain I/LnJ). Positional candidate genes with higher expression in I/LnJ mice are Fxr (official symbol, Nr1h4), encoding the nuclear bile salt receptor, on chromosome 10 and Shp1 (official symbol, Nr0b2), encoding the small heterodimer partner 1, on chromosome 4. A significant locus associated with gallstone score on chromosome 17, named Lith9 (susceptibility allele conferred by strain PERA/Ei), colocalizes with the genes Abcg5 and Abcg8 that encode the canalicular cholesterol transporter. Higher hepatic messenger RNA expression of Abcg5 and Abcg8 in strain PERA/Ei correlates positively with higher biliary cholesterol levels. Conclusions: Our findings suggest a primary role of the nuclear bile salt receptor FXR and the canalicular cholesterol transporter ABCG5/ABCG8 in the genetic susceptibility and pathogenesis of cholesterol cholelithiasis in these strains of inbred mice.