Abstract

One of the most perplexing but fascinating segments of the mouse genome is the t complex, a 12–15 cM region of Chromosome 17. A number of alternative allelic combinations called t haplotypes characterize this segment. Wild-derived t haplotypes affect a wide variety of biological properties including embryogenesis, male fertility, male transmission ratio, meiotic recombination, and tail length (Silver 1985). Since the discovery of t haplotypes 55 years ago (Dobrovoloskaia-Zavadskaia and Kobozieff 1932), many investigators have tried to account for this diverse array of attributes. It is evident that t haplotypes carry mutant alleles at loci such as tct (t complex tail) that interacts with the dominant mutation T (brachyury) to produce tailless offspring, tcr (t complex responder) and tcd-1 through tcd-4 (t complex distorter) that interact to distort transmission ratio in t/+ males (Lyon 1984, 1987; Silver and Remis 1987), tcs-1 through tcs-3 (t complex sterility) that cause male sterility (Lyon 1986, 1987), and recessive lethal mutations that map to 16 different loci and that affect different stages of embryonic development (Bennett 1975; Klein et al., 1984).

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