Pas7^A/JOlaHsd
QTL Variant Detail

Summary

• QTL variant: Pas7^A/JOlaHsd
• Name: pulmonary adenoma susceptibility 7; A/JOlaHsd
• MGI ID: MGI:2445575
• QTL: Pas7 Location: Chr18:72745594-84144595 bp Genetic Position: Chr18, cM position of peak correlated region/allele: 45.88 cM
• QTL Note: genome coordinates based on the marker associated with the peak LOD score

Variant origin

• Strain of Specimen: A/JOlaHsd

Variant description

• Allele Type: QTL
• Mutation: Undefined
• This allele confers susceptibility to lung tumors compared to BALB/cOlaHsd. (J:50533)
• Inheritance: Not Specified

Expression

In Structures Affected by this Mutation:

1 anatomical structure(s)

Notes

Homozygous animals exhibit increased tumor multiplicity.

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

J:50533

One hundred fifty-one (A/JO1aHsd x BALB/cOlaHsd)F2 and 49 and 52 BALB/c and A/J backcross mice were used to localize quantitative trait loci involved with susceptibility to the chemical induction of lung adenomas. A/J mice are highly susceptible to the induction of lung tumors by urethane; BALB/c mice are relatively resistant. Four or possibly five QTLs associated with increased susceptibility to the development of lung adenomas were identified in this study.

QTL Pas8, pulmonary adenoma susceptibility 8, mapped to a 12.6 cM interval on Chromosome 1 between markers D1Mit102 and D1Mit33 with a peak LOD score of 3.0. at D1Mit33. Pas8 accounted for 40.0% of trait variance in a model including both genotype and sex as each locus.

QTL Pas9, pulmonary adenoma susceptibility 9, mapped to a 40.4 cM interval on Chromosome 4 between markers D4Mit39 and D4Mit77 with a peak LOD score of 6.4 at D4Mit77. Pas9 accounted for 39% of the trait variance in a model including both genotype and sex as each locus.

A possible QTL, Pas1c, pulmonary adenoma susceptibility 1c, mapped to Chromosome 6 with marker D6Mit263. This locus mapped 37.0 cM proximal to Kras and increased tumor multiplicity about threefold in male mice homozygous for the BALB/c allele compared with those homozygous for the A/J allele. With a LOD score of 1.0 its existance was determined uncertain.

QTL Pas5b, pulmonary adenoma susceptibility 5b, mapped to Chromosome 11 between markers D11Mit161 and D11Mit54 with a peak LOD score of 3.2 at marker D11Mit54. Pas5b was attributed with 37% of trait variance in a model including both genotype and sex as each locus.

QTL Pas10, pulmonary adenoma susceptibility 10, mapped to Chromosome 13 with marker D13Mit279.

QTL Pas7, pulmonary adenoma susceptibility 7, mapped to Chromosome 18 in an 8.4 cM interval between markers D18Mit4 and D18Mit188 with a LOD score of 15.1 at D18Mit188. Tumor multiplicity was increased at this locus in males and females with genotypes AA, AC and CC. Pas7 accounted for 59% of trait variance in the same model.

Mice with the AA genotype had significantly more tumors than those with AC or CC genotypes at Pas8, Pas5b and Pas7, but at Pas9 and Pas1c strain A/J carried the resistant allele. Alleles were generally additive, though there was possible dominance at the Chr 1 locus, with some evidence for a slight interaction between the Pas9 (Chr4) and the Pas5b (Chr11), loci.

References

• Original: J:50533 Festing MF, et al., At least four loci and gender are associated with susceptibility to the chemical induction of lung adenomas in A/J x BALB/c mice. Genomics. 1998 Oct 15;53(2):129-36
• All: 1 reference(s)