Estq2^C3H/HeJ
QTL Variant Detail

Summary

• QTL variant: Estq2^C3H/HeJ
• Name: estradiol regulated response QTL 2; C3H/HeJ
• MGI ID: MGI:2156160
• QTL: Estq2 Location: Chr5:32634084-32634190 bp Genetic Position: Chr5, cM position of peak correlated region/allele: 17.33 cM
• QTL Note: genome coordinates based on the marker associated with the peak LOD score

Variant origin

• Strain of Specimen: C3H/HeJ

Variant description

• Allele Type: QTL
• Mutation: Undefined
• This allele confers decreased uterine weight compared to C57BL/6J.
• Inheritance: Not Specified

Notes

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

J:52898

Significant strain differences in several of the estradiol-regulated uterotropic responses have been observed suggesting that they may be genetically controlled. In this study, the authors addressed the question whether uterine growth, as determined by wet weight, is a genetically controlled phenotype. C57BL/6J and (C57BL/6J x C3H/HeJ)F1 mice responded with a greater increase in wet weight than did C3H/HeJ mice. The authors used a [(C57BL/6J x C3H/HeJ)F1 x C3H/HeJ] backcross to identify QTLs associated with uterine growth.

Statistical analysis of the data identified as 2.39 cM region on Chromosome 5 between D5Mit296 and D5Mit388 that is significant ([a] = 0.05, threshold value = 13.39). This locus was designated as Estq2.

Mice with C57BL/6J alleles atthe Estq2 and Estq3loci show the greatest increase in uterine weight. Putative candidates in this region include the Htr5a and Il6 genes. A model including the Estq2 locus, Estq3 locus and the interaction term between Estq3 and D10Mit180 was significant in explaining the QTLassociated with uterine weight (F = 14.256; P^0.0001). This model explained 30.7% of the variation in uterine weight. This supported the hypothesis of interaction between QTL controlling estradiol-regulated responses.

References

• Original: J:52898 Roper RJ, et al., Interacting quantitative trait loci control phenotypic variation in murine estradiol-regulated responses. Endocrinology. 1999 Feb;140(2):556-61
• All: 1 reference(s)