| First Author | Herrmann BG | Year | 1999 |
| Journal | Nature | Volume | 402 |
| Issue | 6758 | Pages | 141-6 |
| PubMed ID | 10647005 | Mgi Jnum | J:58548 |
| Mgi Id | MGI:1349207 | Doi | 10.1038/45970 |
| Citation | Herrmann BG, et al. (1999) A protein kinase encoded by the t complex responder gene causes non-mendelian inheritance [see comments]. Nature 402(6758):141-6 |
| abstractText | Males heterozygous for the t-haplotype form of mouse chromosome 17 preferentially transmit the t-chromosome to their progeny. Several distorter/sterility loci carried on the t-haplotype together impair flagellar function in all spermatozoa whereas the responder, Tcr, rescues t-sperm but not wild-type sperm. Thus, t-sperm have an advantage over wild-type sperm in fertilizing egg cells. We have isolated Tcr by positional cloning and show that it is a member of a novel protein kinase gene family, designated Smok, which is expressed late during spermiogenesis. Smok kinases are components of a signal cascade which may control sperm motility. Tcr has a reduced kinase activity, which may allow it to counterbalance a signalling impairment caused by the distorter/sterility loci. Tcr transgene constructs cause non-mendelian transmission of chromosomes on which they are carried, which leads to sex-ratio distortion when Tcr cosegregates with the Y chromosome. |
