Mapping Data

Experiment

• Experiment
  TEXT-Congenic
• Chromosome
  12
• Reference
  J:152405 Kurey I, et al., Distinct genetic control of parasite elimination, dissemination, and disease after Leishmania major infection. Immunogenetics. 2009 Sep;61(9):619-33
• ID
  MGI:4360546

Genes

Gene	Assay Type
Lmr22	resistance/susceptibility
D12Mit37	PCR amplified length variant

Notes

• Experiment
  In the present study the genetics of disease symptoms, immunological parameters and parasite load in draining lymph nodes and in the spleen following Leishmania major infection were analyzed.
  
  A special tool for the genetic analysis of multigenic traits, recombinant congenic strains, were used. Each of the 20 CcS/Dem RC mouse strains carries a different random subset of 12.5% genes of the resistant donor strain STS/A (STS) on the background of the susceptible strain BALB/cHeA (BALB/c). Two hundred and ninty nine (BALB/c x CcS11/Dem)F2 mice were used (155 were females and 144 were males). The CcS11 strain was in more than 38 generations of inbreeding.
  
  The CcS11 strain differs from BALB/c at STS-derived segments on eight chromosomes. These differential segements were typed in the F2 hybrid mice between BALB/c and CcS11 using 16 mircosatellite markers with a maximal interval between any two markers of 19 cM. Linkage analysis of the F2 hybids indicated four novel loci on Chromosomes 1, 7, 12, 16, and additional effects for a previoulsy detected locus on Chromosome 10.
  
  Lmr22, leishmaniasis resistance 22, mapped to Chromosome 12 of CcS11/Dem with marker D12Mit37 at 1.0 cM. Lmr22 was detected in interaction with Lmr32f (D10Mit12), p=0.0269,
  influencing IL-4 concentrations. The interaction accounted for 7.71% of trait variation.
  The highest and lowest levels of IL-4 were observed in BALB/c and STS/A homozygotes, respectively, at both loci.