Apmt2^I/LnJ
QTL Variant Detail

Summary

• QTL variant: Apmt2^I/LnJ
• Name: accelerator of polyoma-induced mammary tumors 2; I/LnJ
• MGI ID: MGI:2157319
• QTL: Apmt2 Location: unknown Genetic Position: Chr9, cM position of peak correlated region/allele: 53.48 cM
• QTL Note: genome coordinates based on the marker associated with the peak LOD score

Variant origin

• Strain of Specimen: I/LnJ

Variant description

• Allele Type: QTL
• Mutation: Undefined
• This allele confers increased mammary tumor susceptibility compared to FVB/NJ. (J:64663)
• Inheritance: Other (see notes)

Expression

In Structures Affected by this Mutation:

1 anatomical structure(s)

Notes

Apmt1 and Apmt2 participate in epistatic interactions. Animals homozygous for FVB/NJ-derived alleles at Apmt1 and heterozygous at Apmt2 exhibit the highest incidence of mammary tumors.

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

J:64663

A genome wide scan using 69 markers was initiated to find loci responsible for tumor acceleration in mice. A total of 126 female mice from FVB/N females X (I/LnJ females X FVB/N-TgN(MMTVPyVT)^634mul males) F1 males were informative. A region of mouse Chromosome 9 including D9Mit182 was correlated with an acceleration of tumorignensis.

References

• Original: J:64663 Le Voyer T, et al., An epistatic interaction controls the latency of a transgene-induced mammary tumor. Mamm Genome. 2000 Oct;11(10):883-9
• All: 1 reference(s)