Abmm^BALB/cByJ
QTL Variant Detail

Summary

• QTL variant: Abmm^BALB/cByJ
• Name: antibody mediated myocarditis; BALB/cByJ
• MGI ID: MGI:3032986
• QTL: Abmm Location: Chr12:110264461-110264573 bp Genetic Position: Chr12, cM position of peak correlated region/allele: 60.56 cM
• QTL Note: genome coordinates based on the marker associated with the peak LOD score

Variant origin

• Strain of Specimen: BALB/cByJ

Variant description

• Allele Type: QTL

Notes

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

J:52296

79 polymorphic markers were screened in 120 (BALB/cByJ x DBA/2J)F1 x DBA/2J backcross animals to identify loci associated with susceptibility to antibody-mediated autoimmune myocarditis. Following injection of myosin-specific antibodies, inbred strain DBA/2J develops myocarditis while inbred strain BALB/cJ is resistant to myocarditis. (BALB/cByJ x DBA/2J)F1 hybrid animals are resistant to myocarditis. A locus was detected on mouse Chromosome 12, Abmm (antibody-mediated myocarditis susceptibility), from 43 cM - 63 cM with peak significance P<0.0001 at D12Mit133. DBA/2J-derived alleles contribute to increased susceptibility to myocarditis 12-fold in female animals and 5-fold in all animals at this locus. Several candidate genes are found in this 15 cM interval: Serpina1 (Spi1), Serpina3kr, Serpina3k, Gsc, Bdkrb2, Ckb, Dnahc13, Dync1h1, Iap3rc18, Iaprc6, Traf3, Tnfaip2 (Tnfip2), Mse1, and Igh. Suggestive loci were also detected on mouse Chromosome 9 (P = 0.0014 at D9Mit19) at 38 cM and on distal mouse Chromosome1 (P =0.0003). Heterozygosity at the Chromosome 9 locus contributes to increased susceptibility to myocarditis, while homozygosity at the Chromosome 1 locus for DBA/2J-derived alleles contributes to increased susceptibility to myocarditis only in male animals.

References

• Original: J:52296 Kuan AP, et al., Genetic control of autoimmune myocarditis mediated by myosin-specific antibodies [published erratum appears in Immunogenetics 1999 Jun;49(6):595-6]. Immunogenetics. 1999 Feb;49(2):79-85
• All: 1 reference(s)