ABSTRACT
Mouse t haplotypes are variant forms of chromosome 17 that can be transmitted at non-Mendelian ratios by heterozygous +/t males. The accumulated genetic data indicate that ’ +-sperm’ and ‘t-sperm’ are produced in equal numbers but that most ‘+-sperm’ are rendered dysfunctional, so that ‘t-sperm’ have a relative advan-tage at fertilization. To date, the basis for this t-induced sperm dysfunction has remained unknown. Here we demonstrate that a high proportion of sperm obtained from certain strains of +/t mice undergo a premature acrosome reaction under in vitro capacitation conditions.
The simplest interpretation of these data, in conjunction with previous results, is that developing ‘+-spermatids’ are preprogrammed by ‘i-spermatids’ to undergo this premature reaction. Since acrosome-reacted sperm are unable to participate in the process of fertilization, this defect could account for the extreme distortion of transmission ratio observed from mice heterozygous for a class of complete t haplotypes.
