Mapping Data

Experiment

• Experiment
  TEXT-QTL
• Chromosome
  17
• 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:3624758

Genes

Gene	Assay Type
Sxbq3	visible phenotype
D17Mit21	PCR amplified length variant
H2	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 17, significant linkage to total serum IgG at 12 and 24 weeks of age mapped to D17Mit21 (18.64 cM) between H2-K and H2-A (LOD=5.8 and 5.5, respectively; 8% and 8% of variance, respectfully). This locus is named Sxbq3 (SGC/Knj cross B6 QTL 3). Sxbq3 also shows significant linkage to vasculitis (LOD=3.2; 5% of variance). C57BL/6Slc-derived alleles at Sxbq3 confer increased IgG with a dominant mode of inheritance, while heterozygosity at Sxbq3 confers increased vasculitits severity. H2 is a potential candidate gene for Sxbq3. A suggestive locus for glomerulonephritis mapped 11 cM distal to Sxbq3 at D17Mit88 (LOD=2.9).