Mapping Data

Experiment

• Experiment
  TEXT-Congenic
• Chromosome
  16
• 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:4360547

Genes

Gene	Assay Type
Lmr23	resistance/susceptibility
D16Mit73	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.
  
  Lmr23, leishmaniasis resistance 23, mapped to Chromosome 16 of CcS11/Dem with marker D16Mit73 at 8.6 cM. Lmr23 was detected in an interaction with Lmr20c (D1Mit403) influencing IFN gamma concentrations, p=0.0201 and accounting for 6.93% of trait variance.
  The highest level of IFN gamma was observed in STS/A homozygotes at both loci. [Table 6.]