Mapping Data

Experiment

• Experiment
  TEXT-QTL
• Chromosome
  1
• Reference
  J:106521 Su Z, et al., Quantitative Trait Locus Analysis of Atherosclerosis in an Intercross Between C57BL/6 and C3H Mice Carrying the Mutant Apolipoprotein E Gene. Genetics. 2006 Mar;172(3):1799-807
• ID
  MGI:3628441

Genes

Gene	Assay Type
Bodwt1	visible phenotype
D1Mit425	PCR amplified length variant
D1Mit270	PCR amplified length variant
Apoa2	reported elsewhere
Soat1	reported elsewhere

Notes

• Experiment
  Linkage analysis was performed on 234 female animals from a (C57BL/6J-Apoe^tm1Unc x C3H/HeJ-Apoe^tm1Unc)F2 intercross to identify QTLs associated with atherosclerotic lesion size, plasma lipids, and body weight. Animals were place on a Western diet at 6 weeks of age for a duration of 12 weeks. On a Western diet, parental strain C3H/HeJ-Apoa^tm1Unc exhibits 6-fold increased plasma HDL cholesterol and 10-fold increased aortic lesion size compared to parental strain C57BL/6J. 130 polymorphic markers at an average spacing of 13 cM were used for the genome scan.
  
  Significant linkage to plasma lipids and body weight mapped to 2 peaks on distal mouse Chromosome 1. These 2 linkages are collectively named Bodwt1 (body weight 1). Marker D1Mit425 at 81.6 cM is linked to plasma LDL/VLDL cholesterol (LOD=5.7), triglycerides (LOD=2.5), and body weight (LOD=9). Marker D1Mit270 at 92.3 cM is linked to plasma LDL/VLDL cholesterol (LOD=6.3), HDL cholesterol (LOD=3), and triglycerides (LOD=3.8). C3H/HeJ-derived alleles at Bodwt1 confer increased HDL cholesterol, triglycerides, and body weight with dominant inheritance, and increased LDL/VLDL cholesterol with codominant inheritance. Previously identified QTL Bw17 (75 cM), Bw8q1 (100 cM), Cq2 (100 cM), and Hdlq15 (104 cM)map near this locus. Apoa2 (92.6 cM) and Soat1 (81.6 cM) are potential candidate genes for Bodwt1.
  
  Significant linkage to atherosclerotic lesion size mapped to a broad region of mouse Chromosome 9. This QTL is named Ath29 (atherosclerosis 29). Three peaks are detected within Ath29 at D9Mit206 (20 cM, LOD=2.9, 11% of variance), D9Mit360 (35 cM, LOD=3.7, 24% of variance), and D9Mit156 (42 cM, LOD=4.1, 34% of variance). C57BL/6J-derived alleles at Ath29 confer increased atherosclerotic lesion size with dominant inheritance, while C3H/HeJ-derived alleles confer smaller lesion size with recessive inheritance.
  
  Significant linkage to body weight mapped to 29.8 cM on mouse Chromosome 17 near D17Mit180 (LOD=3.4). This locus is named Bodwt2 (body weight 2). C57BL/6J-derived alleles at Bodwt2 confer increased body weight with recessive inheritance. Previously identified body weight QTL Wt3q3 (14 cM) maps near this locus.
  
  Suggestive linkage to atherosclerotic lesion size mapped to 20 cM on mouse Chromosome 11 near D11Mit236 (LOD=2.4). This locus explains 5% of the variance. C3H/HeJ-derived alleles at D11Mit236 confer decreased atherosclerotic lesion size with a dominant mode of inheritance.
  
  Suggestive linkage to plasma LDL/VLDL cholesterol mapped to 68 cM on mouse Chromosome 5 near D5Mit95 (LOD=2.2) and 56 cM on mouse Chromosome 9 near D9Mit15 (LOD=2.5).
  
  Suggestive linkage to plasma HDL cholesterol mapped to 58.8 cM on mouse Chromosome 3 near D3Mit42 (LOD=2.3).
  
  Suggestive linkage to triglycerides mapped to 41 cM on mouse Chromosome 8 near D8Mit41 (LOD=3.2). Previously identified triglyceride QTLs Tgl1 (51.5 cM) and Trigq2 (30 cM) map near this locus.
  
  Suggestive linkage to body weight mapped to 66 cM on mouse Chromosome 4 near D4Mit251 (LOD=2.7). This locusoverlaps with Bw7 at 59 cM. Suggestive linkage to body weight also mapped to 54 cM on mouse Chromosome 14 near D14Mit185 (LOD=2.2). This locus overlaps with Bwnd2wk7 at 52 cM.