| First Author | Yamazaki D | Year | 2016 |
| Journal | Biochem Biophys Res Commun | Volume | 474 |
| Issue | 3 | Pages | 441-446 |
| PubMed ID | 27150626 | Mgi Jnum | J:235469 |
| Mgi Id | MGI:5796440 | Doi | 10.1016/j.bbrc.2016.05.001 |
| Citation | Yamazaki D, et al. (2016) Complementary role of CNNM2 in sperm motility and Ca(2+) influx during capacitation. Biochem Biophys Res Commun 474(3):441-6 |
| abstractText | Ca(2+) plays a central role in the regulation of sperm motility. We recently reported an unexpected role of CNNM4, a Mg(2+) transporter, in this process by demonstrating perturbed Ca(2+) influx and gradual loss of motility of Cnnm4-deficient sperm. However, Cnnm4-deficient male mice were not entirely infertile, and a significant Ca(2+) response was still observed in their sperm. In the present study, we generated Cnnm4-deficient mice harboring a non-functional Cnnm2 allele (Cnnm2(Delta)), to examine whether CNNM2 compensates for the lost function of CNNM4 in sperm. Cnnm2(+/Delta); Cnnm4(Delta/Delta) mice were infertile, and no obvious histological abnormalities were noted in their testis and epididymis. Their sperm showed normal morphology, but became immotile much more rapidly than those from Cnnm4(Delta/Delta) mice. When capacitation was initiated using serum albumin application, a rapid increase of intracellular Ca(2+) levels was observed in most wild-type sperm, but only about half of sperm from Cnnm4(Delta/Delta) mice exhibited a Ca(2+) response, and the response rate was further reduced in sperm from Cnnm2(+/Delta); Cnnm4(Delta/Delta) mice. Thus, sperm motility and Ca(2+) response were more severely affected in sperm from Cnnm2(+/Delta); Cnnm4(Delta/Delta) mice than in those from Cnnm4(Delta/Delta) mice, implicating CNNM2 in regulating these processes. |
