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首页> 外文期刊>Cell Reports >MIWI2 as an Effector of DNA Methylation and Gene Silencing in Embryonic Male Germ Cells
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MIWI2 as an Effector of DNA Methylation and Gene Silencing in Embryonic Male Germ Cells

机译：MIWI2作为胚胎男性生殖细胞中DNA甲基化和基因沉默的效应子。

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During the development of mammalian embryonic germ cells, global demethylation and de novo DNA methylation take place. In mouse embryonic germ cells, two PIWI family proteins, MILI and MIWI2, are essential for the de novo DNA methylation of retrotransposons, presumably through PIWI-interacting RNAs (piRNAs). Although piRNA-associated MIWI2 has been reported to play critical roles in the process, its molecular mechanisms have remained unclear. To identify the mechanism, transgenic mice were produced; they contained a fusion protein of MIWI2 and a zinc finger (ZF) that recognized the promoter region of a type A LINE-1 gene. The ZF-MIWI2 fusion protein brought about DNA methylation, suppression of the type A LINE-1 gene, and a partial rescue of the impaired spermatogenesis of MILI-null mice. In addition, ZF-MIWI2 was associated with the proteins involved in DNA methylation. These data indicate that MIWI2 functions as an effector of de novo DNA methylation of the retrotransposon.
机译：在哺乳动物胚胎生殖细胞的发育过程中，发生了整体脱甲基和从头DNA甲基化。在小鼠胚胎生殖细胞中，两个PIWI家族蛋白MILI和MIWI2对于逆转座子从头DNA甲基化至关重要，大概是通过PIWI相互作用的RNA（piRNA）。尽管据报道与piRNA相关的MIWI2在该过程中起关键作用，但其分子机制仍不清楚。为了鉴定其机制，产生了转基因小鼠。它们含有MIWI2和锌指（ZF）的融合蛋白，该蛋白识别A LINE-1型基因的启动子区域。 ZF-MIWI2融合蛋白引起DNA甲基化，抑制A型LINE-1基因并部分挽救MILI无小鼠的精子发生。另外，ZF-MIWI2与参与DNA甲基化的蛋白质有关。这些数据表明MIWI2充当反转录转座子从头DNA甲基化的效应子。

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