Mapping Data

Experiment

• Experiment
  TEXT
• Chromosome
  11
• Reference
  J:88853 Lan H, et al., Distinguishing covariation from causation in diabetes: a lesson from the protein disulfide isomerase mRNA abundance trait. Diabetes. 2004 Jan;53(1):240-4
• ID
  MGI:3041083

Genes

Gene	Assay Type
D11Mit48	PCR amplified length variant
P4hb	reported elsewhere

Notes

• Experiment
  108 (C57BL/6J x BTBR.V(B6)-Lep^ob/WiscJ)F2 intercross animals were genotyped at 191 polymorphic loci (average spacing = 20 cM) to identify QTLs associated with differences in P4hb (Pdi) mRNA expression. Parental strain BTBR.V(B6)-Lep^ob/WiscJ is severely diabetic and expresses 20-fold more P4hb mRNA than diabetes resistant strain C57BL/6J. Authors sought to correlate Pdi expression with the diabetes phenotype.
  
  A single locus mapped to 77 cM on mouse Chromosome 11 near D11Mit48 (LOD=30). This is 3 cM upstream of P4hb at 80 cM. BTBR-derived alleles confer increased P4hb mRNA expression with dominant inheritance. Sequence analysis of P4hb revealed several polymorphism between C57BL/6J and BTBR.V(B6)-Lep^ob/WiscJ but these differences do not result in changes to the amino acid sequence or predicted mRNA secondary structure.
  
  Authors conclude that the regulation of P4hb is cis-regulated and does not relate to the diabetes susceptibility phenotype.