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Interacting Quantitative Trait Loci Control Phenotypic Variation in Murine Estradiol-Regulated Responses¹

Department of Veterinary Pathobiology (R.J.R., C.T.) and University Laboratory High School (A.W.M., R.E.B.), University of Illinois at Urbana-Champaign, Urbana, Illinois 61802; the Department of Microbiology, Brigham Young University (J.S.G.), Provo, Utah 84602; the Department of Obstetrics and Gynecology, University of Pennsylvania School of Medicine (C.R.L.), Philadelphia, Pennsylvania 19104; and the Departments of Agronomy and Statistics, Purdue University (R.W.D.), West Lafayette, Indiana 47907

Address all correspondence and requests for reprints to: Dr. Cory Teuscher, Department of Veterinary Pathobiology, 2001 South Lincoln Avenue, Urbana, Illinois 61802. E-mail: cteusche{at}staff.uiuc.edu

The steroid hormone estradiol (E₂) elicits a spectrum of systemic and uterotropic responses in vivo. For example, E₂ treatment of ovariectomized adult and sexually immature rodents leads to uterine leukocytic infiltration, cell proliferation, and organ growth. E₂-regulated growth is also associated with a variety of normal and pathological phenotypes. Historically, the uterine growth response has been used as the key model to understand the molecular and biochemical mechanisms underlying E₂-dependent growth. In this study, genome exclusion mapping identified two quantitative trait loci (QTL) in the mouse, Est2 and Est3 on chromosomes 5 and 11, respectively, that control the phenotypic variation in uterine wet weight. Both QTL are linked to a variety of E₂-regulated genes, suggesting that they may represent loci within conserved gene complexes that play fundamental roles in mediating the effects of E₂. Interaction and multiple trait analyses using the uterine leukocyte response and wet weight suggest that Est4, a QTL on chromosome 10, may encode an interacting factor that influences the quantitative variation in both responses. Our results show that E₂-dependent responses can be genetically controlled and that a genetic basis may underlie the variation observed in many E₂-dependent phenotypes.

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