This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Greenfeld, C. R Articles by Flaws, J. A Search for Related Content PubMed PubMed Citation Articles by Greenfeld, C. R Articles by Flaws, J. A

BAX is involved in regulating follicular growth, but is dispensable for follicle atresia in adult mouse ovaries

¹ Departments of Physiology, ² 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, ⁴ Department of Physiology, University of Arizona, Tucson, Arizona 85715, USA and ⁵ Department of Veterinary Biosciences, University of Illinois, Urbana, Illinois 61802, USA

Correspondence should be addressed to J A Flaws Department of Veterinary Biosciences, University of Illinois, Urbana, Illinois 61802, USA; Email: jflaws{at}uiuc.edu

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 of Bax deletion on follicle growth and death. We observed that the Bax deletion results in delayed vaginal opening and altered follicular growth. Young adult Bax-deficient ovaries contained increased numbers of primordial follicles and a trend towards reduced numbers of growing follicles. Bax deficiency 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, Bax deficiency 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.

This article has been cited by other articles:

				P. A. Fowler, N. J. Dora, H. McFerran, M. R. Amezaga, D. W. Miller, R. G. Lea, P. Cash, A. S. McNeilly, N. P. Evans, C. Cotinot, et al. In utero exposure to low doses of environmental pollutants disrupts fetal ovarian development in sheep Mol. Hum. Reprod., May 1, 2008; 14(5): 269 - 280. [Abstract] [Full Text] [PDF]

				K. Mayo, L. Jameson, and T. K. Woodruff Eggs in the Nest Endocrinology, August 1, 2007; 148(8): 3577 - 3579. [Full Text] [PDF]