NOBOX deficiency disrupts early folliculogenesis and oocyte-specific gene expression

Science. 2004 Aug 20;305(5687):1157-9. doi: 10.1126/science.1099755.


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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

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


  • Homeodomain Proteins
  • Og2x protein, mouse
  • Transcription Factors