Mapping Data

Experiment

• Experiment
  TEXT-Congenic
• Chromosome
  16
• Reference
  J:108764 Havelkova H, et al., Genetics of susceptibility to leishmaniasis in mice: four novel loci and functional heterogeneity of gene effects. Genes Immun. 2006 Apr;7(3):220-33
• ID
  MGI:3625978

Genes

Gene	Assay Type
Lmr18	resistance/susceptibility
Lmr18a	resistance/susceptibility
Lmr18b	resistance/susceptibility
D16Mit7	PCR amplified length variant
Lmr12b	resistance/susceptibility
Lmr12c	resistance/susceptibility
D16Mit126	PCR amplified length variant

Notes

• Experiment
  Disease phenotypes associated with Leishmania major infection were mapped in animals from (CcS-16 x BALB/cHeA)F2 and (CcS-20 x BALB/cHeA)F2 intercross populations. CcS-16 and CcS-20 are recombinant congenic (RC) strains derived from STS/A and BALB/cHeA. Animals were infected with Leishmania major after 9 weeks of age and sacrificed 8 weeks post-infection.
  
  F2 hybrids between BALB/c and CcS20/Dem and F2 hybrids between BALB/c and CcS16 were tested from clinical and immunological consequences post infection. They were genotyped with mircosatellite markers covering the STS-derived segments. Linkage analysis of differing pathological and immunological parameters indicated novel loci and novel functions for previously mapped loci.
  
  In the (BALB/c x CcS20)F2 intercross a novel QTL, Lmr18 was linked with D16Mit7. It was assocaited with two traits:
  Lmr18a was associated with spontaneous proliferation of spleen cells at D16Mit7, corrected p=0.00071. BALB/c alleles at this locus were associated with lower proliferation post infection.
  Lmr18b mapping with D16Mit7 was identified in interaction with Lmr16 at D2Mit52, corrected p=0.0012. Homozygous BALB/c alleles at Lmr18b and homozygous STS/A alleles at Lmr16 interacted to increase spontaneous proliferation of spleen cells post infection.
  
  In the (BALB/c x CcS16) F2 intercross an interaction was identified in the (BALB/c x CcS16)F2 intercross bewteen Lmr19 (D10Mit67) and Lmr12 mapping with marker D16Mit126.
  
  03.28.2016 Curator Note: Lmr12 was previously mapped using the same intercross population used here in J:82717. However, since a different phenotype was measured in that study we have we have labeled the QTL identified in this study as Lmr12b and Lm12c.
  
  Lmr19 (D10Mit67) was identified in interaction with Lmr12c (D16Mit126), p=0.00142.
  A combination of homozygous BALB/c alleles at Lmr19 (D10Mit67) and homozygous STS/A alleles at Lmr12c (near D16Mit126) increase the spontaneous proliferation of spleen cells in infected mice. The Lmr19-Lmr12b interaction acounted for 8.53% of trait variance.
  
  Lmr12b, an independent QTL, was also linked to D16Mit126. Lmr12b controls the level of IL-4 in serum, p=0.0484. STS/A alleles at this locus are associated with higher levels of IL-4 in serum post infection. Lmr12b accounts for 11.10% of trait variance. [Table 3.]