| First Author | Gross VS | Year | 2002 |
| Journal | Mol Reprod Dev | Volume | 62 |
| Issue | 4 | Pages | 519-24 |
| PubMed ID | 12112586 | Mgi Jnum | J:77797 |
| Mgi Id | MGI:2182649 | Doi | 10.1002/mrd.10140 |
| Citation | Gross VS, et al. (2002) Functional analysis of sperm from c-mos-/- mice. Mol Reprod Dev 62(4):519-24 |
| abstractText | The c-mos protooncogene, which is expressed predominantly in male and female germ cells, is crucial for normal oocyte meiosis and female fertility in mice. Inactivation of c-mos results in abnormal oocyte development and leads to ovarian cysts and tumors in vivo. In contrast to the severe effects of c-mos ablation in females, targeted inactivation of c-mos has not been reported to affect spermatogenesis in male mice. However, previously reported studies of male c-mos(-/-) mice have been limited to histological analyses of testes and in vivo matings, both of which are relatively insensitive indicators of sperm production and function. Therefore, we assayed sperm function of c-mos(-/-) males under in vitro conditions to determine whether the absence of Mos during development affected sperm production or fertilizing ability. We found no significant differences between the number of sperm collected from c-mos(-/-) and wild type mice. Additionally, sperm from c-mos(-/-) and c-mos(+/+) males performed equally well in assays of in vitro fertilization (IVF) and fertilization-associated events including zona pellucida (ZP) penetration, sperm/egg plasma membrane fusion, and sperm chromatin remodeling. Therefore, we suggest that the function of Mos in spermatogenesis is either not related to the ultimate fertilizing potential of the sperm, or else the absence of Mos is masked by a redundant kinase. Mol. Reprod. Dev. 62:519-524, 2002. |
