Foxl2 is required for commitment to ovary differentiation

被引：261

作者：

Ottolenghi, C

Omari, S

Garcia-Ortiz, JE

Uda, M

Crisponi, L

Forabosco, A

Pilia, G

Schlessinger, D ^{[1
]}

机构：

[1] NIA, Genet Lab, Baltimore, MD 21224 USA

[2] George Washington Univ, Grad Program Genet, Washington, DC 20052 USA

[3] Osped Microcitem, Consiglio Nazl Ric, Ist Neurogenet & Neurofarmacol, I-09100 Cagliari, Italy

[4] Univ Modena & Reggio Emilia, Dipartimento Maternoinfantile, Policlin, I-41100 Modena, Italy

来源：

HUMAN MOLECULAR GENETICS | 2005年 / 14卷 / 14期

关键词：

D O I：

10.1093/hmg/ddi210

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Genetic control of female sex differentiation from a bipotential gonad in mammals is poorly understood. We find that mouse XX gonads lacking the forkhead transcription factor Foxl2 form meiotic prophase oocytes, but then activate the genetic program for somatic testis determination. Pivotal Foxl2 action thus represses the male gene pathway at several stages of female gonadal differentiation. This suggests the possible continued involvement of sex-determining genes in maintaining ovarian function throughout female reproductive life.

引用

收藏

页码：2053 / 2062

页数：10

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