| First Author | Yeung CH | Year | 2000 |
| Journal | Biol Reprod | Volume | 63 |
| Issue | 2 | Pages | 612-8 |
| PubMed ID | 10906072 | Mgi Jnum | J:63727 |
| Mgi Id | MGI:1861515 | Doi | 10.1095/biolreprod63.2.612 |
| Citation | Yeung CH, et al. (2000) The cause of infertility of male c-ros tyrosine kinase receptor knockout mice. Biol Reprod 63(2):612-8 |
| abstractText | Male homozygous transgenic c-ros knockout mice are sterile by natural mating, lack a part of their epididymis, and the epididymal sperm exhibit tail angulation in vivo and in vitro. To ascertain if this abnormal tail form caused the infertility, the number and nature of sperm in the tract of females mated to knockout and wild-type mice were determined. Percentage motility and numbers of sperm in the uterus 1 h after mating were similar between genotypes. The majority of the uterine sperm from the wild-type males had straight flagella, whereas 46-86% of knockout sperm were bent at the cytoplasmic droplet even when motile. Motile knockout sperm showed a 54 and 37% reduction in the straightline and curvilinear velocities compared with straight wild-type sperm. Sequential flushings of the oviduct 4 h after mating with the wild-type males contained sperm: 591 +/- 119 free, 371 +/- 70 loosely, and 122 +/- 47 tightly bound to the epithelium, but no knockout sperm were recovered from the oviduct or observed within the uterotubal junction in tissue sections. The infertility of c-ros knockout male mice can be explained by the sperm's inability to enter the oviduct, as a result of their bent tails forming the entangled sperm mass and their compromised flagellar vigor within the uterus. |
