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BAX Is Involved In Regulating Follicular Growth, But Is Dispensable For Follicle Atresia In Adult Mouse Ovaries

Chuck R Greenfeld, Janice K Babus, Priscilla A Furth, Sam Marion, Patricia B Hoyer, Jodi A Flaws

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Mammalian females are endowed with a finite number of primordial follicles at birth or shortly thereafter. Immediately following the formation of the primordial follicle pool, cohorts of these follicles are recruited to begin growth, and this recruitment continues until the primordial follicle population is depleted. Once recruited, a follicle will either grow and ovulate or undergo atresia. Follicle atresia results from the apoptotic death of follicular cells. Members of the BCL-2 family of proteins are important regulators of apoptosis in most cells including in the ovary. Here, we tested the hypothesis that the proapoptotic BAX is an important regulator of follicle survival. We used a variety of histological and biochemical techniques to investigate the impact ofBaxdeletion on follicle growth and death. We observed that theBaxdeletion results in delayed vaginal opening and altered follicular growth. Young adultBax-deficient ovaries contained increased numbers of primordial follicles and a trend towards reduced numbers of growing follicles.Baxdeficiency led to a reduction in average litter size, and also a reduction in the number of oocytes ovulated in response to exogenous gonadotropins. In contrast,Baxdeficiency did not alter follicle atresia. In conclusion, BAX appears to be an important regulator of follicle growth, but is dispensable for follicle atresia in mice.