Foxl2 is required for commitment to ovary differentiation.

نویسندگان

  • Chris Ottolenghi
  • Shakib Omari
  • J Elias Garcia-Ortiz
  • Manuela Uda
  • Laura Crisponi
  • Antonino Forabosco
  • Giuseppe Pilia
  • David Schlessinger
چکیده

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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عنوان ژورنال:
  • Human molecular genetics

دوره 14 14  شماره 

صفحات  -

تاریخ انتشار 2005