| First Author | Hao XX | Year | 2016 |
| Journal | Mol Reprod Dev | Volume | 83 |
| Issue | 7 | Pages | 615-23 |
| PubMed ID | 27265621 | Mgi Jnum | J:316294 |
| Mgi Id | MGI:6835346 | Doi | 10.1002/mrd.22664 |
| Citation | Hao XX, et al. (2016) Selective deletion of Smad4 in postnatal germ cells does not affect spermatogenesis or fertility in mice. Mol Reprod Dev 83(7):615-23 |
| abstractText | SMAD4 is the central component of canonical signaling in the transforming growth factor beta (TGFbeta) superfamily. Loss of Smad4 in Sertoli cells affects the expansion of the fetal testis cords, whereas selective deletion of Smad4 in Leydig cells alone does not appreciably alter fetal or adult testis development. Loss of Smad4 in Sertoli and Leydig cells, on the other hand, leads to testicular dysgenesis, and tumor formation in mice. Within the murine testes, Smad4 is also expressed in germ cells of the seminiferous tubules. We therefore, crossed Ngn3-Cre or Stra8-Cre transgenic mice with Smad4-flox mice to generate conditional knockout animals in which Smad4 was specifically deleted in postnatal germ cells to further uncover cell type-specific requirement of Smad4. Unexpectedly, these germ-cell-knockout mice were fertile and did not exhibit any detectable abnormalities in spermatogenesis, indicating that Smad4 is not required for the production of sperm; instead, these data indicate a cell type-specific requirement of Smad4 primarily during testis development. Mol. Reprod. Dev. 83: 615-623, 2016. (c) 2016 Wiley Periodicals, Inc. |
