van der Heijden Godfried W, Bortvin Alex
Department of Embryology, Carnegie Institution for Science, Baltimore, MD 21218, USA.
Epigenetics. 2009 Feb 16;4(2):76-9. doi: 10.4161/epi.4.2.7783. Epub 2009 Feb 14.
Postmigratory mouse primordial germ cells (PGCs) undergo extensive epigenetic remodeling that includes DNA methylation (DM) reprogramming of imprinted genes and, surprisingly, of transposable elements (TEs). Given the danger posed by TEs to the integrity of the germline, even a brief derepression of TEs is counterintuitive and puzzling. In the male fetal gonocytes, a sophisticated repressive mechanism that uses DM and TE-targeting piRNAs has evolved to stably silence TEs. A recent study has further increased the complexity of this problem by revealing that TE silencing is alleviated specifically at the onset of meiosis in testes lacking MAEL, a piRNA pathway protein. These observations and prior work of others are consistent with existence of an additional reprogramming event, transient relaxation of transposon silencing (TRTS), at the onset of both male and female meiosis in mice. In this Point of View we propose that TE expression is inherent to mammalian meiosis and discuss potential functional significance of this phenomenon.
迁移后的小鼠原始生殖细胞（PGCs）经历广泛的表观遗传重塑，其中包括印记基因的DNA甲基化（DM）重编程，令人惊讶的是，还包括转座元件（TEs）的重编程。鉴于TEs对种系完整性构成的危险，即使是短暂的TEs去抑制也是违反直觉且令人费解的。在雄性胎儿生殖母细胞中，一种复杂的抑制机制已经进化出来，该机制利用DM和靶向TE的piRNA来稳定沉默TEs。最近的一项研究通过揭示在缺乏piRNA途径蛋白MAEL的睾丸中，TE沉默在减数分裂开始时会特异性缓解，进一步增加了这个问题的复杂性。这些观察结果以及其他人之前的研究工作与在小鼠雄性和雌性减数分裂开始时存在另一种重编程事件——转座子沉默的短暂松弛（TRTS）相一致。在本观点中，我们提出TE表达是哺乳动物减数分裂所固有的，并讨论了这一现象的潜在功能意义。
