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

Abstract

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.

Cytonuclear Genic Incompatibilities Cause Increased Mortality in Male F2 Hybrids of Nasonia giraulti and N. vitripennis

“…Selfish genetic elements, for example, are known to transmit themselves at the expense of their homologs (Lyttle 1991;Hurst 1993;Hurst and Werren 2001). Well-studied examples are the Segregation distorter in Drosophila (Ganetsky 1977;Wu et al 1988;Merrill et al 1999) and the t haplotypes in mice (Silver 1993).…”

Mouse biodiversity in the genomic era

“…They produce hybrid sterility phenotypes analogous to those associated with sperm inactivation causing transmission distortion of the t-haplotype. This raises the interesting possibility that these hybrid sterility genes coincide with the t-haplotype distorter genes, and evolved as by-products of the selection exerted by the selfish t-haplotype distorter in the M. musculus lineage (Hurst, 1993). All strong candidates for these distortion/sterility genes encode dynein chains involved in sperm motility, and the role of at least one of them seems to differ between M. spretus and the laboratory mouse .…”