Male sterility of the mouse t-complex is due to homozygosity of the distorter genes.
Evidence is presented that the male sterility produced by the mouse t-complex is due to interaction of at least three sterility factors. These factors are carried in the same partial haplotypes as the three distorter genes, Tcd-1, Tcd-2, and Tcd-3 and are suggested to be identical with them. When heterozygous, the distorter/sterility genes act on the wild-type form of the responder gene, rendering sperm carrying it nonfunctional, thus leading to high transmission of the t form of the responder. When homozygous, the harmful effects of the distorter genes are stronger and affect both forms of the responder, leading to sterility. If homozygous sterility is an inescapable part of ratio distortion, then the t-lethals confer a selective advantage in removing sterile males from the population. Thus, the relationship between the various properties of the t-complex can now be understood.
D000818:Animals; D005796:Genes; D008040:Genetic Linkage; D005838:Genotype; D006720:Homozygote; D007248:Infertility, Male / Q000235:genetics*; D008297:Male; D051379:Mice / Q000235:genetics*