Mapping Data

Experiment

• Experiment
  TEXT-QTL
• Chromosome
  13
• 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:3624672

Genes

Gene	Assay Type
Scgq5	visible phenotype
D13Mit60	PCR amplified length variant
D13Mit144	PCR amplified length variant

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.
  
  Significant linkage to total serum IgM at 12 weeks of age (LOD=4.8; 17% of variance) and total serum IgM and IgG at 24 weeks of age (LOD=6.7 and 4.4, respectively; 27% and 6% of variance, respectfully) mapped to mouse Chromosome 13 between D13Mit60 (16 cM) and D13Mit144 (48 cM). This locus is named Scgq5 (spontaneous crescentic glomerulonephritis QTL 5). SCG/Knj-derived alleles at Scgq5 confer increased IgG and IgM with a recessive mode of inheritance. Previously identified immune QTL mapping near Sgcq5 include Sgp3 (43 cM) and a locus reported by Haywood et al in 2001.