Mapping Data

Experiment

• Experiment
  TEXT-Congenic
• Chromosome
  2
• 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:3625969

Genes

Gene	Assay Type
Lmr28c	resistance/susceptibility
Lmr28d	resistance/susceptibility
Lmr28e	resistance/susceptibility
Lmr28f	resistance/susceptibility
Lmr28g	resistance/susceptibility
D2Mit102	PCR amplified length variant
D2Mit283	PCR amplified length variant
D2Mit389	PCR amplified length variant
Lmr16	resistance/susceptibility
D2Mit52	PCR amplified length variant
Nfatc2	reported elsewhere
Cd40	reported elsewhere

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 locus, Lmr16 mapped to D2Mit52 at 99.0 cM. Lmr16 does not have an effect by itself but interacts with Lmr18b (D16Mit7) on chromosome 16 to affect spontaneous splenocyte proliferation. Nfatc2 (95.5 cM) and Cd40 (97.0 cM) are potential candidate genes for Lmr18b.
  
  In the (BALB/c x CcS16)F2 intercross linkage mapping revealed novel functions for a previoulsy identified QTL, Lmr14.
  
  03.23.2016 Curator Note: Lmr14 was originally identified in J:82717 mapping with D2Mit283 on CcS16. It was identified there only in interaction with Lmr25a influencing IgE levels.In J:82716 using the same mapping population, (BALB/c x CcS16)F2 mice, a broader QTL spanning D2Mit389 at 50.3 cM to D2Mit51 at 95.5 cM was identified and named Lmr28. Lmr14 maps within this region at 83.5 cM. We have equated the individual traits mapped here with the Lmr28 QTL as they map within the broader region using the same mapping population. We have created Lmr28c through Lmr28g to represent the novel functions identified in the current mapping study.
  
  Lmr28c mapped with marker D2Mit102 on Chr 2 and was associated with IFN gamma levels in serum. STS/A alleles at this locus were associated with higher IFN gamma, p=0.0325. This locus accounted for 5.74% of trait variance.
  
  Lmr28d mapping with marker D2Mit102 was detected in interaction with Lmr25b (D10Mit103), p=0.0133. Homozygous STS/A alleles at both loci were associated with higher levels of IL-2. This interaction was attributed to 8.65% of trait variance.
  
  Lmr28e mapping with marker D2Mit283 was detected in interaction with Lmr12 (D16Mit126), p=0.00238. Homozygous BALB/c alleles at both loci were associated with higher TNF alpha levels in serum post infection. Lower levels were detected when homozygous STS/S alleles were at both loci. This interaction was attributed to 6.03% of trait variance.
  
  Lmr28f mapping with marker D2Mit283 was detected in interaction with Lmr29 (D18Mit49), p=0.0261. Homozygous STS/S alleles at both loci were associated with low levels of TNF alpha levels in serum. This interaction was attributed with 7.24% of trait variance.
  
  Lmr28g mapping with D2Mit389 was associated with spontaneous spleen cell proliferation, p=0.0189. BALB/c alleles were associated with higher cell proliferation. Lmr28g was assocaited with 5.11% of trait variance