Safronova L D, Kudriavtsev I V
Severtsov Institute of Ecology and Evolution, Russian Academy of Sciences, Moscow, 117071 Russia.
Genetika. 2001 Sep;37(9):1198-206.
Mouse t-complex located on chromosome 17 contains genes affecting solely male fertility. Some genes of this complex are recessive lethals; nonetheless, the high frequency of the t-complex carriers in a population is maintained due to a mechanism referred to as transmission ratio distortion (TRD), i.e., after crosses with wild-type females, males heterozygous for the t-complex transmit the t-bearing chromosome to nearly all their offspring, which suggests that the t-complex genes control sperm function. Analysis of this phenomenon shows that the resultant TRD is determined by the ratio between the distorter genes (Tcd) and a responder gene (Tcr) located within the t-complex region. Many authors believe that two to six distorter genes currently known have an additive effect. A genetic model of the non-Mendelian inheritance in the progeny of heterozygous male mice specifically explains sterility of animals carrying the t-complex with complementary lethal genes. The model suggests that some distorter gene products interacting with the responder gene have a selective effect on motility of both mutant and wild-type sperm. Insufficient sperm motility and/or their unsuccessful capacitation result in poor if any fertilization. Information on the t-complex genes is necessary for understanding the biological mechanisms of male sterility and may be used in medical practice.
位于17号染色体上的小鼠t复合体包含仅影响雄性生育力的基因。该复合体的一些基因是隐性致死基因；尽管如此，由于一种称为传递比率畸变（TRD）的机制，种群中t复合体携带者的高频率得以维持，即与野生型雌性交配后，t复合体杂合的雄性将携带t的染色体几乎传递给所有后代，这表明t复合体基因控制精子功能。对这一现象的分析表明，产生的TRD由位于t复合体区域内的畸变基因（Tcd）和响应基因（Tcr）之间的比率决定。许多作者认为，目前已知的两到六个畸变基因具有累加效应。杂合雄性小鼠后代中这种非孟德尔遗传的遗传模型特别解释了携带t复合体和互补致死基因的动物的不育性。该模型表明，一些与响应基因相互作用的畸变基因产物对突变型和野生型精子的活力都有选择性作用。精子活力不足和/或它们的获能失败导致受精不良或根本无法受精。关于t复合体基因的信息对于理解雄性不育的生物学机制是必要的，并且可用于医学实践。
