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NOBOX deficiency disrupts early folliculogenesis and oocyte-specific gene expression.

Primordial ovarian follicles in mice form when somatic cells surround individual oocytes. We show that lack of Nobox, an oocyte-specific homeobox gene, accelerates postnatal oocyte loss and abolishes the transition from primordial to growing follicles in mice. Follicles are replaced by fibrous tissue in female mice lacking Nobox in a manner similar to nonsyndromic ovarian failure in women. Genes preferentially expressed in oocytes, including Oct4 and Gdf9, are down-regulated in Nobox-/- mice, whereas ubiquitous genes such as Bmp4, Kit, and Bax remain unaffected. Therefore, Nobox is critical for specifying an oocyte-restricted gene expression pattern essential for postnatal follicle development.

Pubmed ID: 15326356


  • Rajkovic A
  • Pangas SA
  • Ballow D
  • Suzumori N
  • Matzuk MM


Science (New York, N.Y.)

Publication Data

August 20, 2004

Associated Grants

  • Agency: NICHD NIH HHS, Id: HD007165
  • Agency: NICHD NIH HHS, Id: HD01426
  • Agency: NICHD NIH HHS, Id: HD33438
  • Agency: NICHD NIH HHS, Id: HD42500

Mesh Terms

  • Animals
  • Animals, Newborn
  • Apoptosis
  • Embryonic and Fetal Development
  • Female
  • Fertility
  • Gene Deletion
  • Gene Expression Regulation, Developmental
  • Gene Targeting
  • Genes, Homeobox
  • Germ Cells
  • Homeodomain Proteins
  • Male
  • Meiosis
  • Mice
  • Mice, Inbred C57BL
  • Oocytes
  • Oogenesis
  • Ovarian Follicle
  • Ovary
  • Transcription Factors