Mapping Data

Experiment

• Experiment
  TEXT-QTL
• Chromosome
  11
• Reference
  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
• ID
  MGI:1346618

Genes

Gene	Assay Type
D11Mit67
Estq3	visible phenotype
D11Mit132

Notes

• Experiment
  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 a region on Chromosome 11 between D11Mit67 and D11Mit132 that is significant ([a] = 0.10, threshold value = 11.67). This locus was designated as Estq3.
  
  Mice with C57BL/6J alleles at the Estq2 and Estq3 loci show the greatest increase in uterine weight. Putative candidates in this region include the Cola1, Itga3, Csf3, Rara, Thra and the Brca1 genes. A model including the Estq2 locus, Estq3 locus and the interaction term between Estq3 and D10Mit180 was significant in explaining the QTL associated with uterine weight (F = 14.256; P^0.0001). This model explained 30.7% of the variation in uterine weight. Another model based upon multiple linear regression found the independent variables Estq1, D10Mit180 and D16Mit144 as well as the interaction terms between D10Mit180 and Estq1 and between Estq3 and D10Mit180 to be significant (F = 9.026, P^0.0001. This model explained 30.9% of the variation in uterine weight. This supported the hypothesis ofinteraction betweenQTL controlling estradiol-regulated responses.