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 RIS Download
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