A protein kinase encoded by the t complex responder gene causes non-mendelian inheritance

Bernhard G. Herrmann (), Birgit Koschorz, Karin Wertz, K. John McLaughlin and Andreas Kispert
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Bernhard G. Herrmann: Max-Planck-Institute of Immunobiology
Birgit Koschorz: Max-Planck-Institute of Immunobiology
Karin Wertz: Max-Planck-Institute of Immunobiology
K. John McLaughlin: Max-Planck-Institute of Immunobiology
Andreas Kispert: Max-Planck-Institute of Immunobiology

Nature, 1999, vol. 402, issue 6758, 141-146

Abstract: Abstract 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.

Date: 1999
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DOI: 10.1038/45970

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