Semin Reprod Med 2007; 25(4): 252-263
DOI: 10.1055/s-2007-980219
Published in 2007 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA.

Transcriptional Control of Ovarian Development in Somatic Cells

Chris Ottolenghi1 , Maria Colombino1 , Laura Crisponi2 , Antonio Cao2 , Antonino Forabosco3 , David Schlessinger1 , Manuela Uda2
  • 1Laboratory of Genetics, National Institute on Aging, Baltimore, Maryland
  • 2Istituto di Neurogenetica e Neurofarmacologia, Consiglio Nazionale delle Ricerche, c/o Ospedale Microcitemico, Cagliari, Italy
  • 3Genetica Medica, Dipartimento Materno-Infantile, Università di Modena e Reggio-Emilia, Policlinico, Modena, Italy
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Publikationsdatum:
26. Juni 2007 (online)

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ABSTRACT

Developmental transitions of the bipotential gonad to the embryonic ovary and thence to the follicle-filled mature ovary are expected to be coordinated by sets of transcription factors. We infer candidate lists here, focusing on somatic cell fate and function. For the mouse, developmental stages of ovary differentiation are relatively discretely phased, and provide a unique tool to investigate the intricate mechanisms that lead to the acquisition of female reproductive competence. Cross-platform gene expression profiles supplement functional studies of specific genes and comparative information about human biology. Available data suggest that: (1) peak transcription activity just precedes the two most decisive steps of early ovary differentiation (i.e., entry into meiosis and follicle formation); (2) alternating peak gene activities in oocytes and somatic cells may reflect reciprocal interactions; and (3) in addition to stable states of chromatin modification associated with morphogenesis, some features of differentiation are labile, contingent on the expression state of critical factors. Examples are the maintenance of somatic sex determination by continued Foxl2 action and the reversible maintenance of follicles in a quiescent state by nuclear Foxo3.

REFERENCES

David Schlessinger

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eMail: SchlessingerD@grc.nia.nih.gov