Mapping Data

Experiment

• Experiment
  TEXT-QTL
• Chromosome
  4
• Reference
  J:108420 Hamano Y, et al., Genetic dissection of vasculitis, myeloperoxidase-specific antineutrophil cytoplasmic autoantibody production, and related traits in spontaneous crescentic glomerulonephritis-forming/Kinjoh mice. J Immunol. 2006 Mar 15;176(6):3662-73
• ID
  MGI:3624751

Genes

Gene	Assay Type
Sxbq1	visible phenotype
D4Mit71	PCR amplified length variant
Ifna	reported elsewhere
C1qa	reported elsewhere
Tnfrsf1b	reported elsewhere

Notes

• Experiment
  Linkage analysis was performed on 420 female animals from a (C57BL/6Slc x SCG/Knj)F2 intercross to identify QTL for renal phenotypes. Parental strain SCG/Knj is derived from BXSB/Mp and MRL/Mp-Fas^lpr, and spontaneously develops crescentic glomerulonephritis and vascularitis. The Fas-^lpr mutation is largely responsible for the disease phenotype but this experiment seeks to identify non-Fas disease-associated loci. 102 polymorphic markers covering 85% of the genome at a 20 cM resolution was used for the genome scan. F2 animals were analyzed by cohorts grouped according to genotype at the Fas locus.
  
  On mouse Chromosome 4, significant linkage to total serum IgM at 12 and 24 weeks of age was detected at 61.9 cM near D4Mit71 (LOD=5.7-6.8; 8%-10% of the variance). This locus is named Sxbq1 (SGC/Knj cross B6 QTL 1). C57BL/6Slc-derived alleles at Sxbq1 confer increased total IgM with an additive mode of inheritance. Previously identified renal QTL mapping to chromosome 4 include Sle2 (38 cM), Lbw2 (42.6 cM), Nba1 (75 cM), Lxw1 (6.5 cM), Arvm2 (58 cM), and Asm2 (51 cM). Ifna (formerly Ifa; 42.6 cM), C1qa (formerly C1q; 66.1 cM), and Tnfrsf1b (formerly Tnfr2; 75.5 cM) are potential candidate genes for Sxbq1.