Mapping Data

Experiment

• Experiment
  TEXT-Congenic
• Chromosome
  10
• 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:4360548

Genes

Gene	Assay Type
Lmr32	resistance/susceptibility
Lmr32a	resistance/susceptibility
Lmr32b	resistance/susceptibility
Lmr32c	resistance/susceptibility
Lmr32d	resistance/susceptibility
Lmr32e	resistance/susceptibility
Lmr32f	resistance/susceptibility
D10Mit12	PCR amplified length variant
D10Mit46	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, Lmr5.
  
  03.30.2016 Curator Note: Because Lmr5 was originally mapped in J:82715 using a (BALB/c x CcS5 mapping population, which differs from the mapping population used here, we consider the current study a separate mapping experiment and have named the QTL identified here as, Lmr32. leishmaniasis resistance 32. We have also assigned distinct nomenclature to the individual disease phenotypes that mapped with significance to Lmr32, creating Lmr32a through Lmr32f. Lmr32 represents the collection of individual traits analyzed that map to this same locus.
  
  Lmr32 maps to Chr10 of CcS11/Dem with markers D10Mit12 at 56.0 cM and D10Mit46 at 63.0 cM.
  
  Lmr32a is linked with marker D10Mit12; this locus influences parasite load in spleens, p=0.00539 and accounts for 4.54% of trait variation. BALB/c alleles are associated with higher parasite numbers at this locus. [Table 3.]
  
  Lmr32b is also linked with marker D10Mit12; this locus influences the severity of splenomegaly, p0.000698 and accounts for 11.60% of trait variance. BALB/c alleles at this locus are assoicated with more severe splenomegaly after infection. [Table 3.]
  
  Lmr32c is linked with D10Mit12, p=0.0000527 and D10Mit46, p=0.0000483 and influences skin lesion size post infection. BALB/c alleles at this locus are associated with larger skin lesions. [Table 4.]
  
  Lmr32d is linked with marker D10Mit12; this locus influences IgE serum concentrations, p=0.0302 and accounts for 4.70% of trait variance. BALB/c alleles at this locus are associated with higher IgE levels post infection. [Table 5.]
  
  Lmr32e is linked with marker D10Mit12 and was detected influencing IFN gamma levels in interaction with Lmr21b (D17Mit67), p=0.0195. Lmr32e accounted for 7.18% of trait variance. Lowest IFN gamma levels were observed either in STS/A homozygotes at both loci or in BALB/c homozygotes at both loci. [Table 7.]
  
  Lmr32f, also linked with D10Mit12, was detected influencing IL-4 levels in serum in interaction with Lmr22 (D12Mit37), p=0.0269. Lmr32f accounted for 7.71% of trait variance.
  The highest and lowest level of IL-4 was observed in BALB/c and STS/A homozygotes, respectively. [Table 8.]