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Premature ovarian failure in androgen receptor-deficient mice.


ABSTRACT: Premature ovarian failure (POF) syndrome, an early decline of ovarian function in women, is frequently associated with X chromosome abnormalities ranging from various Xq deletions to complete loss of one of the X chromosomes. However, the genetic locus responsible for the POF remains unknown, and no candidate gene has been identified. Using the Cre/LoxP system, we have disrupted the mouse X chromosome androgen receptor (Ar) gene. Female AR(-/-) mice appeared normal but developed the POF phenotype with aberrant ovarian gene expression. Eight-week-old female AR(-/-) mice are fertile, but they have lower follicle numbers and impaired mammary development, and they produce only half of the normal number of pups per litter. Forty-week-old AR(-/-) mice are infertile because of complete loss of follicles. Genome-wide microarray analysis of mRNA from AR(-/-) ovaries revealed that a number of major regulators of folliculogenesis were under transcriptional control by AR. Our findings suggest that AR function is required for normal female reproduction, particularly folliculogenesis, and that AR is a potential therapeutic target in POF syndrome.

SUBMITTER: Shiina H 

PROVIDER: S-EPMC1324980 | biostudies-literature | 2006 Jan

REPOSITORIES: biostudies-literature

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Premature ovarian failure in androgen receptor-deficient mice.

Shiina Hiroko H   Matsumoto Takahiro T   Sato Takashi T   Igarashi Katsuhide K   Miyamoto Junko J   Takemasa Sayuri S   Sakari Matomo M   Takada Ichiro I   Nakamura Takashi T   Metzger Daniel D   Chambon Pierre P   Kanno Jun J   Yoshikawa Hiroyuki H   Kato Shigeaki S  

Proceedings of the National Academy of Sciences of the United States of America 20051222 1


Premature ovarian failure (POF) syndrome, an early decline of ovarian function in women, is frequently associated with X chromosome abnormalities ranging from various Xq deletions to complete loss of one of the X chromosomes. However, the genetic locus responsible for the POF remains unknown, and no candidate gene has been identified. Using the Cre/LoxP system, we have disrupted the mouse X chromosome androgen receptor (Ar) gene. Female AR(-/-) mice appeared normal but developed the POF phenotyp  ...[more]

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