Figure 7.

Model for mouse t phenotypes based on dynein–axoneme interactions. In all cases, the distorter gene (d) products, which are dynein subunits, are free to diffuse (arrows) through the intercellular bridges that connect developing spermatids. However, the responder gene (Tcr) product quickly assembles onto the axoneme and thus remains associated with the nucleus that encoded it. Wild-type and t-encoded proteins are indicated by open and filled symbols, respectively. t-encoded dyneins contain mutations that affect their assembly and/or function; the t-encoded responder contains mutations that affect its ability to bind t-encoded dyneins. (A) In developing spermatids of heterozygous +/t mice, the mutated t responder binds only wild-type dyneins, preventing incorporation of mutant dyneins into the axoneme associated with the nucleus carrying the t haplotype. In contrast, the wild-type responder binds both wild-type and mutant dyneins; the mutant dyneins “poison” the axoneme into which they are incorporated. As a result, the sperm bearing the t haplotype has slightly impaired motility (because of the presence of the mutant responder), but the sperm with the wild-type homologue has greatly impaired motility. The sperm bearing the t haplotype is much more likely to reach and fertilize an egg, thus leading to transmission ratio distortion. (B) In spermatids of homozygous t/t mice, all dyneins produced are defective and bind poorly to the t-encoded responder. The resulting sperm are nonmotile, and the mice are sterile. (In this case, all spermatids are identical, so only one is shown.) (C) In mice containing a partial t haplotype with a t-encoded responder, but no t-encoded distorters, only wild-type dyneins are produced and assembled into the axonemes. Sperm carrying Tcr^t and sperm carrying Tcr⁺ are both motile, although the former will suffer a competitive disadvantage because of the presence of the t-encoded responder in their axonemes.