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Human Molecular Genetics Advance Access originally published online on June 8, 2005
Human Molecular Genetics 2005 14(14):2053-2062; doi:10.1093/hmg/ddi210
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Published by Oxford University Press 2005

Foxl2 is required for commitment to ovary differentiation

Chris Ottolenghi1, Shakib Omari1,2, J. Elias Garcia-Ortiz1, Manuela Uda3, Laura Crisponi3, Antonino Forabosco4, Giuseppe Pilia3 and David Schlessinger1,*

1Laboratory of Genetics, National Institute on Aging, Baltimore, MD 21224, USA, 2Graduate Genetics Program, The George Washington University, Washington, DC 20052, USA, 3Istituto di Neurogenetica e Neurofarmacologia, Consiglio Nazionale delle Ricerche, c/o Ospedale Microcitemico, Cagliari 09100, Italy and 4Genetica Medica, Dipartimento Materno-Infantile, Università di Modena e Reggio-Emilia, Policlinico, Modena 41100, Italy

* To whom correspondence should be addressed. Tel: +1 4105588337; Fax: +1 4105588331; Email: schlessingerd{at}grc.nia.nih.gov

Received March 21, 2005; Accepted June 2, 2005

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.


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