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Mapping Data
Experiment
  • Experiment
    TEXT-QTL
  • Chromosome
    17
  • Reference
    J:106112 Smith JD, et al., Atherosclerosis susceptibility loci identified from a strain intercross of apolipoprotein E-deficient mice via a high-density genome scan. Arterioscler Thromb Vasc Biol. 2006 Mar;26(3):597-603
  • ID
    MGI:3618888
Genes
GeneAlleleAssay TypeDescription
Ath26 resistance/susceptibility
Notes
  • Experiment
    QTL associated with atherosclerosis susceptibility on a CHOW diet were mapped in 209 (DBA/2J-Apoetm1Bres x AKR/J-Apoetm1Bres)F2 animals. Linkage analysis was performed using 1967 single nucleotide polymorphic (SNP) markers. Parental strain DBA/2J-Apoetm1Bres exhibits significantly greater aortic root lesion area compared to AKR/J-Apoetm1Bres, and females exhibit higher susceptibility than males.

    Linkage to aortic lesion area mapped to 14 cM on mouse Chromosome 15 (LOD=3.29 at rs13482467) in 95 female F2 animals. This locus explains 17.9% of the phenotypic variance and is named Ath22 (atherosclerosis 22). DBA/2J-derived alleles at Ath22 confer atherosclerosis susceptibility in females.

    Suggestive linkage to aortic lesion area in female F2 animals mapped to 33 cM on chromosome 3 (LOD=2.73 at rs13477166), 84 cM on chromosome 5 (LOD=2.59 at rs13478585), and 26 cM on chromosome 13 (LOD=2.5 at rs13481782). These loci are designated Ath23, Ath24, and Ath25, respectively. AKR/J-derived alleles at Ath23 confer increased lesion size in females with dominant inheritance, and this locus explains 12.7% of the variance. DBA/2J-derived alleles at Ath24 confer increased lesion size in females with codominant inheritance explaining 15.1% of the variance. Ath24 also shows significant linkage to lesion area in pooled male and female F2 animals (LOD=5.49). Heterozygosity for DBA/2J- and AKR/J-derived alleles at Ath25 confers increased lesion size in females.

    Linkage to aortic lesion area mapped to 20 cM on mouse Chromosome 17 near rs13482966 (LOD=4.25) in 114 F2 male animals. This locus is named Ath26 (atherosclerosis 26). AKR/J-derived alleles at Ath26 confer increased lesion size in males with a dominant mode of inheritance. This locus explains 14.5% of the variance. Linkage was also detected at 22 cM on mouse Chromosome 18 (Ath27) near rs13483316 (LOD=3.58), and at 107 cM on mouse Chromosome 2 (Ath28) near rs13476938 (LOD=3.28). Heterozygosity for DBA/2J- and AKR/J-derived alleles at Ath27 confers increased lesion size in males while DBA/2J-derived alleles at Ath28 confer increased lesion size in males with a codominant mode of inheritance. Ath28 explains 11% of the variance.



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last database update
11/19/2024
MGI 6.24
The Jackson Laboratory