A model for the mechanism of transmission ratio distortion and for t-associated hybrid sterility.

A mechanistic model is presented to account for the action of t-complex of mice. This model takes account of recent evidence suggesting that t-complex distorters are amorphs or hypomorphs. Following Lyon's (Genet. Res. 59, 27 (1992) scheme, the model proposes that the t-complex distorter (tcd+) loci for normal function than does the wild-type form of tcr. However, a tradeoff against this ability to drive is a reduced efficiency of the haploid specific product of tcrt in the absence of drive. Regulation of tcr could be achieved by differential splicing or post-translational modification under the control of the t-complex distorters. It is shown that the model is consistent with known fertility and distortion data, as well as with the finding that the mechanism of drive is intimately connected with the mechanism of intraspecific homozygous sterility. Importantly, the model predicts that the mechanism of hybrid sterility associated with the t-complex is the same as the mechanism of intraspecific homozygous sterility. If accepted then this will be, to the best of the author's knowledge, the first description and characterization of a Haldane rule sterility gene. The new understanding of the mechanisms of t-complex shows its mode of operation to be fundamentally different to the only other well-described autosomal meiotic driver, Segregation Distorter (SD) of Drosophila melanogaster.