Choice of sex in animal breeding? Excess of male progeny from males carrying mouse responder transgene on Y chromosome

Cloning of the responder, a gene transmitted at up to 95% from male carriers to their progeny, showed that it encodes a novel protein kinase likely to control sperm motility. The gene can effectively be used to manipulate the transmission of autosomes or sex chromosomes. In the latter case, an excess of male or female offspring can be generated. The study was reported by a research group at the Max Planck Institute for Immunbiology in the 11 November issue of Nature.

The mouse t complex responder (Tcr) affects the transmission of the chromosome carrying it from males to their progeny whereas normally chromosomes are inherited at equal ratio. A high transmission ratio of Tcr (up to 95%) requires the action of additional mutant factors, the distorters (D1 to D5), while Tcr alone (on a wild type background) is transmitted at a low ratio (e.g. 17%).

Cloning of Tcr showed that it encodes a mutant form of a member of a novel protein kinase gene family, Smok, expressed during spermiogenesis, the process transforming round haploid spermatids into motile sperm cells. Smok kinases, Tcr and the distorters are probably involved in the control of sperm flagellar movement. The distorters affect the motility of sperm cells, the responder counterbalances the negative effect of the distorters and rescues normal sperm motility, but only in those spermatozoa carrying the responder gene. This creates a functional difference between the sperm cells carrying the responder and those lacking it, resulting in an advantage of Tcr sperm in reaching the eggs, and in distortion of the transmission ratio.

The transmission ratio distortion phenomenon is associated with the t complex, a large region of chromosome 17 which exists in two different forms in wild mouse populations. Transmission ratio distortion has been known for several decades and has been studied extensively by several generati

Contact: Bernhard Herrmann

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