Mapping Data

Experiment

• Experiment
  TEXT-QTL
• Chromosome
  1
• Reference
  J:78027 Bagot S, et al., Identification of two cerebral malaria resistance loci using an inbred wild-derived mouse strain. Proc Natl Acad Sci U S A. 2002 Jul 23;99(15):9919-23
• ID
  MGI:2669991

Genes

Gene	Assay Type
Berr1	resistance/susceptibility
D1Mit203	PCR amplified length variant
D1Mit462	PCR amplified length variant
D1Mit221	PCR amplified length variant
Tgfb2	reported elsewhere

Notes

• Experiment
  Genome scan was performed on 190 (WLA/Pas x C57BL/6JRj)F1 x C57BL/6JRj backcross animals using 132 microsatellite markers at an average spacing of 11 cM to identify QTLs associated with resistance to experimental cerebral malaria (ECM). Following infection with Plasmodium berghei, parental strain WLA/Pas is resistant to cerebral malaria but succumbs to hyperparasitemia after 11-25 days. Parental strain C57BL/6J is susceptible to cerebral malaria.
  
  Significant linkage was detected on mouse Chromosome 1 and mouse Chromosome 11. These loci were named Berr1 (berghei resistance locus 1) and Berr2 (berghei resistance locus 2), respectively. These 2 loci jointly affect resistance to cerebral malaria.
  
  Berr1 maps from 87.2 cM (D1Mit203) to 107.3 cM (D1Mit462) onmouse Chromosome 1 with peak linkage at 102 cM (D1Mit221, P=1.3 x 10-5). WLA/Pas-derived alleles appear to confer resistance to cerebral malaria at this locus. Tgfb2 maps to 101.5 cM on chromosome 1 and is a possible candidate gene for Berr1. Tgfb2 levels have been inversely correlated to the severity of malaria infections in mice.
  
  Berr2 spans a 7 cM region on mouse Chromosome 11 with peak linkage at 75 cM (D11Mit338, P=4.8 x 10-5). WLA/Pas-derived alleles appear to confer resistance to cerebral malariaat this locus.
  
  Suggestive linkage to ECM was detected on mouse Chromosome 14 at 25 cM (D14Mit113, P=1.4 x 10-3).