lla^AKR/JMs
QTL Variant Detail

Summary

• QTL variant: lla^AKR/JMs
• Name: lymphoma latency acceleration; AKR/JMs
• MGI ID: MGI:3044408
• QTL: lla Location: unknown Genetic Position: Chr17, Syntenic

Variant origin

• Strain of Specimen: AKR/JMs

Variant description

• Allele Type: QTL
• Inheritance: Dominant

Notes

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

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. A recessive allele in SL/Kh mice shortened the development of lymphomas and was shown to be dependent on H2 haplotypes. 114 (AKR/JMs x SL/Kh)F2 mice were analyzed for the segregation of the shortened latency phenotype (lla) as a quantitative trait. The results from the F2 cross show that the lla phenotype was significantly associated with H2 class II loci with a maximal LOD score of 7.06.

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:41197 Hiai H, et al., To be or not to be a T-lymphomas, that is determined by a dominant gene Tlsm-1 in mouse models. Leukemia. 1997 Apr;11 Suppl 3:193-4
• All: 2 reference(s)