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Genes and Development
Vol. 11, No. 17,
pp. 2153-2162,
September 1, 1997
in
female reproduction
Eukaryotic Transcriptional Regulation Group and
1 Special
Program in Germline Mutation, Advanced Bioscience Laboratories, Inc.
(ABL)-Basic Research Program, National Cancer Institute
(NCI)-Frederick Cancer Research and Development Center,
Frederick, Maryland 21702-1201 USA
A large number of intercellular signaling molecules have been
identified that orchestrate female reproductive physiology. However,
with the exception of steroid hormone receptors, little information
exists about the transcriptional regulators that mediate cellular
responses to these signals. The transcription factor C/EBP
(CCAAT/enhancer-binding
protein ) is expressed in ovaries and
testes, as well as many other tissues of adult mice. Here we show that
mice carrying a targeted deletion of the C/EBP gene
exhibit reproductive defects. Although these animals develop normally
and males are fertile, adult females are sterile. Transplantation of
normal ovaries into mutant females restored fertility, thus localizing
the primary reproductive defect to the ovary proper. In normal ovaries,
C/EBP mRNA is specifically induced by luteinizing hormone (LH/hCG) in the granulosa layer of preovulatory
antral follicles. C/EBP-deficient ovaries lack corpora
lutea and fail to down-regulate expression of the prostaglandin
endoperoxidase synthase 2 and P450 aromatase genes in response to
gonadotropins. These findings demonstrate that C/EBP
is essential for periovulatory granulosa cell differentiation in
response to LH. C/EBP is thus established as a
critical downstream target of G-protein-coupled LH receptor signaling
and one of the first transcription factors, other than steroid hormone
receptors, known to be required for ovarian follicle development in
vivo.
[Key Words:
C/EBP knockout; granulosa
cells; ovulation; corpus luteum; ovary; female reproduction]
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