Mapping Data

Experiment

• Experiment
  TEXT-QTL
• Chromosome
  2
• 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:3624661

Genes

Gene	Assay Type
Scgq3	visible phenotype
D2Mit26	PCR amplified length variant
D2Mit213	PCR amplified length variant
Il1	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 by Fas genotype status.
  
  On mouse Chromosome 2, Scgq3 shows significant linkage to total serum IgG at 24 weeks of age with LOD=4.8 between D2Mit26 (84 cM) and D2Mit213 (105 cM). This locus explains10% of the phenotypic variance. SCG/Knj-derived alleles at Scgq3 confer increased serum IgG with a recessive mode of inheritance. Il1 at 73 cM is a potential candidate gene for Scgq3.