| First Author | Yeung CH | Year | 1998 |
| Journal | J Reprod Fertil Suppl | Volume | 53 |
| Pages | 137-47 | PubMed ID | 10645273 |
| Mgi Jnum | J:60040 | Mgi Id | MGI:1352562 |
| Citation | Yeung CH, et al. (1998) Receptor tyrosine kinase c-ros knockout mice as a model for the study of epididymal regulation of sperm function. J Reprod Fertil Suppl 53:137-47 |
| abstractText | Despite recent advances in understanding sperm function and characterization of epididymal secretion products, little is known about the mechanisms regulating the fertilizing capacity of spermatozoa during maturation. The recently produced receptor tyrosine kinase c-ros knockout mouse has provided the first transgenic model for such study. The only abnormalities in these transgenic mice are shown in homozygous mutant males whose epididymis fails to develop the initial segment. Normal matings by these mice do not result in oocyte fertilization, but in vitro fertilization is successful. Detailed analysis of the development of sperm motility per se did not reveal any gross abnormalities that could explain infertility in vivo. Studies on c-ros, which is expressed temporarily in a few embryonic organs but solely and at high levels in the epididymis in adults, are few and nothing is known about its putative ligand or substrates. Review of the literature on other family members of receptor tyrosine kinases throws hardly any light on its role in epididymal function affecting sperm maturation. The preliminary observations that the majority of motile spermatozoa exhibit angulation in the tail and further findings suggest a defect in the volume regulation mechanism which would normally develop during sperm maturation. This finding has provided a starting point for further research to establish the link between abnormal epididymides and sterility. |
