Underdeveloped uterus and reduced estrogen responsiveness in mice with disruption of the estrogen-responsive finger protein gene, which is a direct target of estrogen receptor alpha

The biological roles of estrogen-responsive finger protein (efp) in vivo we re evaluated in mice carrying a loss-of-function mutation in efp by gene-ta rgeted mutagenesis. Although efp homozygous mice were viable and fertile in both sexes, the uterus that expressed abundant estrogen receptor alpha exh ibited significant underdevelopment. When the ovariectomized homozygotes we re subjected to 17 beta-estradiol treatment, they showed remarkably attenua ted responses to estrogen, as exemplified by decreased interstitial water i mbibition and retarded endometrial cell increase, at least, attributable to the lower ratio of G1 to S-phase progression in epithelial cells. These re sults suggest that efp is essential for the normal estrogen-induced cell pr oliferation and uterine swelling as one of the direct targets of estrogen r eceptor alpha.