Tlsm1^AKR/JMs
QTL Variant Detail

Summary

• QTL variant: Tlsm1^AKR/JMs
• Name: thymic lymphoma susceptible 1; AKR/JMs
• MGI ID: MGI:2156830
• QTL: Tlsm1 Location: Chr7:122250663-135170901 bp Genetic Position: Chr7, cM position of peak correlated region/allele: 81.27 cM
• QTL Note: genome coordinates based on the marker associated with the peak LOD score

Variant origin

• Strain of Specimen: AKR/JMs

Variant description

• Allele Type: QTL
• Mutation: Undefined
• This allele confers susceptibility to T-lymphomas compared to SL/Kh. (J:21741)
• Inheritance: Dominant

Notes

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

J:21741

The expression of T lymphomas is under the control of the gene Tlsm1 in AKR mice. In (AKR/Ms x SL/Kh)F1 x SL/Kh backcross mice, significant linkage disequilibrium was found when comparing this gene with microsatellite markers D7Mit32, D7Mit40, D7Mit8 andD7Mit13 on Chromosome 7. Tlsm1 is localized between D7Mit8 and D7Mit13 at a position 7 cM distal to D7Mit8. The penetrance of Tlsm1 is incomplete.

J:41197

SL/Kh is an inbred strains exhibiting high incidence of spontaneous pre-B lymphomas and AKR/JMs is an inbred strain exhibiting high incidence of T-lymphomas.The expression of T lymphomas is under the control of the gene Tlsm1 in AKR/Ms mice. In (AKR/JMs x SL/Kh)F1 x SL/Kh backcross, significant linkage was found when comparing Tlsm1 with microsatellite markers D7Mit71 and D7Mit13. The linkage results suggest that Tlsm1 maps within a segment of mouse Chromosome 7 bounded by cM positions 62 and 70.

J:33016

Linkage analysis was performed on 114 animals from a (SL/Kh x AKR/JMs)F2 intercross to identify loci associated with lymphoma susceptibility. F2 mice were generated by mating reciprocal F1 hybreds bewteen SL/Kh and AKR/Ms. 45 polymorphic markers covering 67% of the mouse genome were used in the analysis.

A locus named Tlsm1 (thymic lymphoma susceptibility 1) mapped to 60 cM mouse Chromosome 7 near D7Mit8. AKR/JMs-derived alleles at Tlsm1 confer susceptibility to thymic lymphomas with a dominant mode of inheritance.

An SL/Kh-derived recessive locus at 18.6 cM on mouse Chromosome 17 near D17Mit21 was found to accelerate the latency period of all types of lymphomas (LOD=7.06). This locus is named lla (lymphoma latency acceleration.) lla overlaps with the H2 locus.

References

• Original: J:21741 Yamada Y, et al., T lymphomagenesis is determined by a dominant host gene thymic lymphoma susceptible mouse-1 (TLSM-1) in mouse models. J Exp Med. 1994 Dec 1;180(6):2155-62
• All: 3 reference(s)