Véron Nathalie, Bauer Hermann, Weisse Andrea Y, Lüder Gerhild, Werber Martin, Herrmann Bernhard G
Department of Developmental Genetics, Max-Planck-Institute for Molecular Genetics, 14195 Berlin, Germany.
Genes Dev. 2009 Dec 1;23(23):2705-10. doi: 10.1101/gad.553009.
The t complex responder (Tcr) encoded by the mouse t haplotype is able to cause phenotypic differences between t and + sperm derived from t/+ males, leading to non-Mendelian inheritance. This capability of Tcr contradicts the concept of phenotypic equivalence proposed for sperm cells, which develop in a syncytium and actively share gene products. By analyzing a Tcr minigene in hemizygous transgenic mice, we show that Tcr gene products are post-meiotically expressed and are retained in the haploid sperm cells. The wild-type allele of Tcr, sperm motility kinase-1 (Smok1), behaves in the same manner, suggesting that Tcr/Smok reveal a common mechanism prone to evolve non-Mendelian inheritance in mammals.
由小鼠t单倍型编码的t复合体应答者（Tcr）能够导致t/+雄性小鼠产生的t精子和+精子之间出现表型差异，从而导致非孟德尔遗传。Tcr的这种能力与为在合胞体中发育并积极共享基因产物的精子细胞所提出的表型等效概念相矛盾。通过分析半合子转基因小鼠中的Tcr小基因，我们发现Tcr基因产物在减数分裂后表达，并保留在单倍体精子细胞中。Tcr的野生型等位基因，即精子运动激酶-1（Smok1），表现方式相同，这表明Tcr/Smok揭示了一种在哺乳动物中易于进化出非孟德尔遗传的共同机制。
