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Submitted on August 20, 2003
Accepted on November 11, 2003
1 Department of Internal Medicine, Division of Endocrinology and Metabolism, Department of Pharmacology, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Blvd., Dallas, Texas 75390-8857, USA
* To whom correspondence should be addressed. E-mail: stephen.hammes{at}utsouthwestern.edu.
Female fertility requires precise regulation of oocyte meiosis. Oocytes are arrested early in the meiotic cycle until just before ovulation, when ovarian factors trigger meiosis, or maturation, to continue. Although much has been learned about the late signaling events that accompany meiosis, until recently less was known about the early actions that initiate maturation. Studies using the well-characterized model of transcription-independent steroid-induced oocyte maturation in Xenopus laevis now show that steroid metabolism, classical steroid receptors, G protein-mediated signaling, and novel G protein-coupled receptors, all may play important roles in regulating meiosis. Furthermore, steroids appear to promote similar events in mammalian oocytes, implying a conserved mechanism of maturation in vertebrates. Interestingly, testosterone is a potent promoter of mammalian oocyte maturation, suggesting that androgen actions in the oocyte might be partially responsible for the polycystic ovarian phenotype and accompanying infertility associated with high androgen states such as polycystic ovarian syndrome or congenital adrenal hyperplasia. A detailed appreciation of the steroid-activated signaling pathways in frog and mammalian oocytes may therefore prove useful in understanding both normal and abnormal ovarian development in humans.
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