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Regular Article |
b Departments of Epidemiology/Preventive Medicine,
c Anatomy/Neurobiology, and
d Medicine, University of Maryland School of Medicine, Baltimore, Maryland 21201
e National Institute of Allergy and Infectious Diseases, Frederick, Maryland 21702
ABSTRACT
Little is known about the embryonic factors that regulate the size of the primordial follicle endowment at birth. A few studies suggest that members of the B-cell lymphoma/leukemia-2 (bcl-2) family of protooncogenes may be important determinants. Thus, the purpose of this study was to test whether bcl-2 regulates the size of the primordial follicle pool at birth. To test this hypothesis, three lines of transgenic mice (c-kit/bcl-2 mice) were generated that overexpress human bcl-2 in an effort to reduce prenatal oocyte loss. The overexpression was targeted to the ovary and appropriate embryonic time period with the use of a 4.8-kilobase c-kit promoter. This promoter provided two to three times more expression of bcl-2 in the ovaries with minimal or no overexpression in most nongonadal tissues. On Postnatal Days 8–60, ovaries were collected from homozygous c-kit/bcl-2 and nontransgenic littermates (controls) and processed for histological evaluation of follicle numbers. All lines of c-kit/bcl-2 mice were born with significantly more primordial follicles than control mice (P
0.05). By Postnatal Days 30–60, however, there were no significant differences in follicle numbers between c-kit/bcl-2 and control mice. These results indicate that bcl-2 overexpression increases the number of primordial follicles at birth, but that the surfeit of primordial follicles is not maintained in postnatal life. These data suggest that it is possible that the ovary may contain a census mechanism by which excess numbers of primordial follicles at birth are detected and removed from the ovary by adulthood.
First decision: 3 November 2000.
1 Supported by National Institutes of Health grant HD38955 to J.A.F., grant CA68033 to P.A.F., and grant AG13844 to A.N.H.
2 Correspondence: Jodi A. Flaws, University of Maryland School of Medicine, Department of Epidemiology and Preventive Medicine, 660 W. Redwood Street, Baltimore, MD 21201. FAX: 410 706 1503; jflaws{at}epi.umaryland.edu
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