Mapping Data

Experiment

• Experiment
  TEXT-QTL
• Chromosome
  7
• 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:3624671

Genes

Gene	Assay Type
Scgq4	visible phenotype
D7Mit117	PCR amplified length variant
D7Mit80	PCR amplified length variant
Coro1a	reported elsewhere
Cd22	reported elsewhere
Bax	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.
  
  Scgq4 (spontaneous crescentic glomerulonephritis QTL 4) maps to mouse Chromosome 7 near D7Mit117 (11 cM) and D7Mit80 (18 cM) with LOD=5.4 for total serum IgM at 12 weeks of age. SCG/Knj-derived alleles at Scgq4 confer increased IgM with a recessive mode of inheritance. This locus accounts for 11% of the phenotypic variance. Previously identified renal QTL mapping near Scgq4 include Sle3 (15 cM), Lbw5 (23 cM),Nba5 (23 cM), and Lmb3 (28 cM). Cd22 (9 cM) and Bax (23 cM) are possible candidate genes for Scgq4.