Mapping Data

Experiment

• Experiment
  TEXT-QTL
• Chromosome
  19
• Reference
  J:76127 Dansky HM, et al., A phenotype-sensitizing apoe-deficient genetic background reveals novel atherosclerosis predisposition Loci in the mouse. Genetics. 2002 Apr;160(4):1599-608
• ID
  MGI:2386540

Genes

Gene	Assay Type
Ath16	resistance/susceptibility
D19Mit120
Vldlr	reported elsewhere
Fgf8	reported elsewhere
Csf2ra	reported elsewhere
Prdx3	reported elsewhere

Notes

• Experiment
  Two independent strain intercosses that carry atherosclerosis phenotype-sensitizing Apoe deficiency were performed to reveal artherosclerosis susceptibility loci that are distinct from loci linked to lipoprotein levels.
  
  Animals from a C57BL/6J-derived background are susceptible to atherosclerosis and yield several-fold higher aortic lesion scores compared to animals from an FVB/NCr-derived background.
  
  In the first cross, referred to as cross 1, B6.129P2-Apoe^tm1Unc x FVB.129P2-Apoe^tm1Bres F1 mice were crossed and the F1 offspring were intercrossed to create 197 (B6.129P2-Apoe^tm1Unc x FVB.129P2-Apoe^tm1Bres) F2 mice for the QTL analysis. Interval mapping was done with 194 markers at a distance of no more than 10cM.
  
  In the second, confirmatory cross, B6.129P2-Apoe^tm1Unc x FVB.129P2-Apoe^tm1Bres F1 mice were crossed and the F1 offspring were intercrossed to create 186 (B6.129P2-Apoe^tm1Unc x FVB.129P2-Apoe^tm1Bres)F2 mice for QTL analysis. This cross was referred to as cross 2; these mice were genotyped using 127 markers at no more than 10cM intervals.
  
  A QTL observed on Chr 19 in cross 1 but not in cross 2 has been named Ath16. Single marker and interval mapping revealed a peak at D19Mit120 (LOD 3.8 in male F2 mice, no linkage was found in female mice on chromosome 19). FVB/NCr-derived alleles confer increased lesion size in a dominant manner at this locus.
  
  Ath16 is evolutionarily conserved with human chromosomal regions 9q12-21, 9q24 and 10q23-26. Possible candidate genes for Ath16 areVldlr, Fgf8, Csf2ra, and Prdx3.