Mapping Data

Experiment

• Experiment
  TEXT-Congenic
• Chromosome
  17
• Reference
  J:211989 Sohrabi Y, et al., Mapping the genes for susceptibility and response to Leishmania tropica in mouse. PLoS Negl Trop Dis. 2013;7(7):e2282
• ID
  MGI:5708638

Genes

Gene	Assay Type
Ltpr7	resistance/susceptibility
D17Mit130
Ltpr7a	resistance/susceptibility
Ltpr7b	resistance/susceptibility
Ltpr7c	resistance/susceptibility

Notes

• Experiment
  L. tropica causes cutaneous leishmaniasis in humans and it can also visceralize. Experiments with mice revealed that manifestations of the disease after infection with L. tropica were strongly influenced by the geneotype of the host.
  
  Mice from recombinant congenic strain CcS16, derived from a BALB/c-c-STS/A (CcS/Dem) panel, were crossed with BALB/c mice to create two experimental groups. The CcS16 strain carries 12.5% genes from the resistant parental STS/A strain and 87.5% from the susceptible BALB/c strain and is more susceptible to L. tropica than BALB/c mice. CcS16 was in more than 90 generations of inbreeding when used for these experiments.
  
  The first experiment consisted of 111 mice, 51 mice from a (BALB/c x CcS16)F2 cross and 60 mice from the recprical cross, (CcS16 x BALB/c)F2. The second group contained a total of 134 mice, 64 from a (BALB/c x CcS16)F2 cross and 70 mice from the (CcS16 x BALB/c)F2 cross. Both F2 hybrid groups were derived from the same F1 parents. Infected mice from both experimental groups were genotyped and their linkage with pathological symptoms and systemic immune responses were determined, revealing eight Ltrp (Leishmania tropica response) loci. These loci are functionally heterogeneous - each influences a different set of responses to the pathogen.
  
  Ltpr7, Leishmania tropica response 7, was identified in both crosses as a significant locus influencing three different interactions on Chr 17 at D17Mit130 at 57.39 cM.
  
  02.17.2016 Curator Note: We have retained the broader QTL identified in this study as Ltpr7. We have also assigned official nomenclature to each of the independent traits that map with significance within the broader Ltpr7 locus creating Ltpr7a, Ltpr7b and Ltpr7c.
  
  Ltpr7a, on Chr17 at D17Mit130, in interaction with Ltpr5a at D10Mit67, corrected p=0.029 influences splenomegaly at 43 weeks after infection. F2 mice with homozygous BALB/c alleles at Ltpr5a and homozygous STS/A alleles at Ltpr7a have the most sever splenomegaly. This interaction accounts for 7.54% of trait variance. [Table 3.]
  
  Ltpr7b, also at D17Mit130, in interaction with Ltpr3c at D3Mit11 influenced CCL3 serum levels, corrected p=0.014 at week 7 after infection. The largest effect was seen when when homozygous STS/A alleles at Ltpr7b were inherited in combination with homozygous BALB/c alleles at Ltpr3c which caused more than 300 times higher CCL3 serum levels than when Ltpr3c was homozygous for the STS/A alleles. This interaction accounted for 3.33% of trait varaince. [Table 6.]
  
  Ltpr7c, also at D17Mit30, in interaction with Ltpr3e at D3Mit11 influenced CCL5 serum levels, corrected p=0.012 at week 7 after infection. The largest effect was seen when when homozygous STS/A alleles at Ltpr7c were inherited in combination with homozygous BALB/c alleles at Ltpr3e which caused more than 28 times higher CCL5 serum levels than when Ltpr3e was homozygous for the STS/A alleles.This interaction accounted for 3.96% of trait vaiance. [Table 6].