Ath22^AKR/J
QTL Variant Detail

Summary

• QTL variant: Ath22^AKR/J
• Name: atherosclerosis 22; AKR/J
• MGI ID: MGI:3618896
• QTL: Ath22 Location: Chr15:20464652-20464652 bp Genetic Position: Chr15, Syntenic

Variant origin

• Strain of Specimen: AKR/J

Variant description

• Allele Type: QTL
• Inheritance: Recessive

Expression

In Structures Affected by this Mutation:

1 anatomical structure(s)

Notes

Mapping and Phenotype information for this QTL, its variants and associated markers

J:106112

QTL associated with atherosclerosis susceptibility on a CHOW diet were mapped in 209 (DBA/2J-Apoe^tm1Bres x AKR/J-Apoe^tm1Bres)F2 animals. Linkage analysis was performed using 1967 single nucleotide polymorphic (SNP) markers. Parental strain DBA/2J-Apoe^tm1Bres exhibits significantly greater aortic root lesion area compared to AKR/J-Apoe^tm1Bres, 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 95female 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. Ath24also shows significant linkage 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 inmales 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.

References

• Original: 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
• All: 1 reference(s)