Brown J, Cebra-Thomas J A, Bleil J D, Wassarman P M, Silver L M
Department of Biology, Princeton University, New Jersey 08544.
Development. 1989 Aug;106(4):769-73. doi: 10.1242/dev.106.4.769.
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 advantage 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 't-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.
小鼠t单倍型是17号染色体的变异形式，杂合子+/t雄性小鼠可按非孟德尔比例传递。积累的遗传数据表明，“+-精子”和“t-精子”数量相等，但大多数“+-精子”功能失调，因此“t-精子”在受精时具有相对优势。迄今为止，这种t诱导的精子功能障碍的原因尚不清楚。在这里，我们证明，从某些+/t小鼠品系获得的高比例精子在体外获能条件下会发生顶体过早反应。结合先前的结果，对这些数据最简单的解释是，发育中的“+-精细胞”被“t-精细胞”预先编程，从而发生这种过早反应。由于顶体反应的精子无法参与受精过程，这种缺陷可能解释了从一类完整t单倍型杂合子小鼠中观察到的传递比例的极端扭曲。
