| First Author | Toscani A | Year | 1997 |
| Journal | Nature | Volume | 386 |
| Issue | 6626 | Pages | 713-7 |
| PubMed ID | 9109487 | Mgi Jnum | J:39632 |
| Mgi Id | MGI:86986 | Doi | 10.1038/386713a0 |
| Citation | Toscani A, et al. (1997) Arrest of spermatogenesis and defective breast development in mice lacking A-myb. Nature 386(6626):713-7 |
| abstractText | The Myb gene family currently consists of three members, named A-, B- and c-myb. These genes encode nuclear proteins that bind DNA in a sequence-specific manner and function as regulators of transcription. In adult male mice, A-myb is expressed predominantly in male germ cells. In female mice, A-myb is expressed in breast ductal epithelium, mainly during pregnancy-induced ductal branching and alveolar development. We report here that mice homozygous for a germline mutation in A-myb develop to term but show defects in growth after birth and male infertility due to a block in spermatogenesis. Morphological examination of the testes of A-myb-/- males revealed that the germ cells enter meiotic prophase and arrest at pachytene. In adult homozygous null A-myb female mice, the breast epithelial compartment showed underdevelopment of breast tissue following pregnancy and the female mice were unable to nurse their newborn pups. These results demonstrate that A-myb plays a critical role in spermatogenesis and mammary gland development. |
