Mapping Data

Experiment

• Experiment
  TEXT-QTL
• Chromosome
  3
• Reference
  J:63511 Qu WM, et al., Genetic dissection of vasculitis in MRL/lpr lupus mice: a novel susceptibility locus involving the CD72c allele. Eur J Immunol. 2000 Jul;30(7):2027-37
• ID
  MGI:2149559

Genes

Gene	Assay Type
Lprm2	reported elsewhere
D3Mit14
D3Mit42

Notes

• Experiment
  Mapping studies of previously identified QTLs associated with systemic vasculitis were extended with a large population of MRL/MpJ-Tnfrsf6^lpr x (MRL/MpJ-Tnfrsf6^lpr x C3H/HeJ-Tnfrsf6^lpr/Tnfrsf6^lpr)F1 backcross animals (n = 179) and (MRL/MpJ-Tnfrsf6^lpr x C3H/HeJ-Tnfrsf6^lpr/Tnfrsf6^lpr)F2 intercross animals (n = 266). Inbred strain MRL/MpJ-Tnfrsf6^lpr develops severe systemic vasculitis while inbred strain C3H/HeJ-Tnfrsf6^lpr/Tnfrsf6^lpr is resistant. Loci significantly associated with susceptibility to vasculitis mapped to mouse Chromosome 4 at 19.8 cM (Arvm1, LOD = 8.0 at D4Mit89) and 58 cM (Arvm2, LOD = 6.3 at D4Mit147) and to mouse Chromosome 3 at 64 cM (P = 0.00084 at D3Mit14). Arvm1 appears to be a novel locus while Arvm2 is thought tobe identical to a locus mapped by Nakatsuru in 1999,and may share overlap with previously mapped autoimmunity-related QTLs Sle2, Nba1, Lbw2, and Lmb1. The chromosome 3 locus is thought be identical to Lprm2, a locus mapped by Wang in 1997. The 3 QTLs appear to interact in an additive fashion: animals withgenotype MRL/MRL at Arvm1, MRL/MRL at Arvm2, and MRL/C3H at the Chromosome 3 locus develop the most severe vasculitis phenotype. Pax5 and Cd72 are possible candidate genes for Arvm1, and Csf3r and Lck arepossible candidate genes for Avrm2. mRNA expression levels were similar for all 4 genes in parental strains, however multiple mutations were found in the Cd72 coding region of the MRL allele.