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BAX regulates follicular endowment in mice

Department of Physiology, University of Maryland, Baltimore, Maryland 21201, USA, ¹ Department of Biology, Syracuse University, Syracuse, New York, 13244, USA, ² Department of Epidemiology and Preventive Medicine, University of Maryland, Baltimore, Maryland 21201, USA, ³ Department of Oncology, Lombardi Cancer Center, Georgetown University, Washington, District of Columbia 20057, USA and ⁴ Department of Veterinary Biosciences, University of Illinois, Urbana, Illinois 61802, USA

Correspondence should be addressed to J A Flaws; Email: jflaws{at}uiuc.edu

It is believed that the endowment of primordial follicles in mammalian ovaries is finite. Once follicles are depleted, infertility ensues. Thus, the size of the initial endowment has consequences for fertility and reproductive longevity. Follicular endowment is comprised of various processes that culminate with the incorporation of meiosis-arrested oocytes into primordial follicles. Apoptosis is prominent during follicular endowment, and apoptosis regulatory genes are involved in its regulation. Conflicting data exist with regard to the role of the proapoptotic Bcl-2 associated X protein (BAX) in follicular endowment. Therefore, we investigated the role of BAX during follicular endowment in embryonic and neonatal ovaries. We found that BAX is involved in regulating follicular endowment in mice. Deletion of Bax yields increased oocyte numbers in embryonic ovaries and increased follicle numbers in neonatal ovaries when compared with wild-type ovaries. Increased follicular endowment in Bax–/–ovaries is not due to enhanced germ cell viability. Further, it is not due to an increased primordial germ cell (PGC) allotment, a delay in the onset of meiosis, or altered proliferative activity of oogonia. Instead, our data suggest that the regulatory activity of BAX in follicular endowment likely occurs during PGC migration, prior to PGC colonization of the gonad.

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