Bw25^DBA/2J
QTL Variant Detail

Summary

• QTL variant: Bw25^DBA/2J
• Name: body weight QTL 25; DBA/2J
• MGI ID: MGI:5635713
• QTL: Bw25 Location: Chr2:124255676-124255676 bp Genetic Position: Chr2, Syntenic

Variant origin

• Strain of Specimen: DBA/2J

Variant description

• Allele Type: QTL

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 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 mouseChromosome 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.

A number of Body weight QTL were also discovered.

Bw20 mapped to 34 cM (LOD 5.1) on mouse Chr12 peaking at marker rs3662628 with the heterzygous phenotype conferring the highest body weight;

Bw21 mapped to 45 cM (LOD 3.7) on mouse Chr19 peaking at marker rs3023497 with the AKR/J allele conferring the highest body weigth in an additive mode of inheritance.

Bw22 and Bw25 mapped to Chr2 in males at 58 cM (rs13476656) and at 70 cM (rs13476754) in males and females . The Chr 2 QTLs may represent the same locus. Bw22 and Bw25 had LODs scores of 3.17 and 4.17 respectively. The AKR/J alleles conferred higher body weight at both loci.

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)