Lmr15^BALB/cHeA
QTL Variant Detail

Summary

• QTL variant: Lmr15^BALB/cHeA
• Name: leishmaniasis resistance 15; BALB/cHeA
• MGI ID: MGI:2661217
• QTL: Lmr15 Location: Chr11:63319407-81830473 bp Genetic Position: Chr11, cM position of peak correlated region/allele: 39.47 cM
• QTL Note: genome coordinates based on the marker associated with the peak LOD score

Variant origin

• Strain of Specimen: BALB/cHeA

Variant description

• Allele Type: QTL
• Inheritance: Other (see notes)

Expression

In Structures Affected by this Mutation:

1 anatomical structure(s)

Notes

Lmr15 exhibits additive inheritance.

Mapping and Phenotype information for this QTL, its variants and associated markers

J:82716

Susceptibility to Leishmania major infection was analyzed in Recombinant Congenic line CcS/Dem. The CcS/Dem line is derived from BALB/cHeA (Leishmania susceptibility) and STS/A (Leishmania resistant). The genetic control of skin lesions and visceral pathology were analyzed in the most susceptible strain, CcS-16.

576 F2 hybrids between BALB/cHeA and CcS-16 were informative in mapping 3 loci that influence skin lesions or visceral pathology.

Lmr13 was linked with markers D18Mit120 and D18Mit35 both with corrected p values of p<0.00000125).

03.16.2016 Curator Note: While Lmr13 was orignally mapped (J:82717) using the same mapping population that was used in the current study, we consider this a different QTL since a different trait has been analyzed. We have named this QTL Lmr27.

Lmr27 was linked with the development of skin lesions. The STS/A allele was associated with larger lesions post infection at this locus.

Lmr14 which controls splenomegaly and hepatomegaly mapped to Chromosome 2.

03.16.2016 Curator Note: Lmr14 was also originally mapped (J:82717) using the same mapping population that was used in the current study. However, different and multiple phenotypes were analyzed in this study. We have named the broader QTL Lmr28 and have assigned official nomenclature to each of the independent traits mapping with significance within Lmr28 creating Lmr28a and Lmr28b.

Lmr28 mapped to Chromosome 2 spanning markers D2Mit389 and D2Mit51 on CcS16. [Fig 1.] It controls the viceral symptoms, splenomegaly and hepatomegaly. The Il1 complex is a candiate gene [Table 2.].

Lmr28a on Chr 2 mapped with markers D2Mit389 at 50.3 cM, corrected p<0.0177, D2Mit102 at 52.5 cM, corrected p<0.00282 and D2Nds3 at 73.0 cM, corrected p<0.00000728. Lmr28a is linked with splenomegaly. The STS/A alelle is associated larger splenomegaly post infection.

Lmr28b also on Chr 2 mapped with markers D2Mit389 at 50.3 cM, corrected p<0.0168, D2Mit102 at 52.5 cM, corrected p<0.00000348 and D2Nds3 at 73.0 cM, corrected p<0.000000137, D2Mit283 at 83.5 cM, correct p<0.00209 and D2Mit51 at 95.5 cM, corrected p<0.0146. Lmr28b is linked with hepatomegaly. The STS/A alelle is associated with larger hepatomegaly post infection.

Lmr15 mapped to Chromosome 11 with markers D11Mit242 at cM 31.0, corrected p<0.00741 and D11Mit37 at 47.0 cM, corrected p<0.0255. [Fig 2.] The STS/A allele is associated with less pronounced hepatomegaly post infection at this locus.

Nos2, nitric oxide synthase 2 and a cluster of several small inducible cyokines genes are potential candidate genes at Lmr15. [Table 2.]

References

• Original: J:82716 Vladimirov V, et al., Different genetic control of cutaneous and visceral disease after Leishmania major infection in mice. Infect Immun. 2003 Apr;71(4):2041-6
• All: 2 reference(s)