一条不依赖于 MILI 的 piRNA 生物发生途径助力部分生殖系重编程。

Vasiliauskaitė Lina, Vitsios Dimitrios, Berrens Rebecca V, Carrieri Claudia, Reik Wolf, Enright Anton J, O'Carroll Dónal

European Molecular Biology Laboratory (EMBL), Monterotondo, Italy.

MRC Centre for Regenerative Medicine, School of Biological Sciences, University of Edinburgh, Edinburgh, UK.

Nat Struct Mol Biol. 2017 Jul;24(7):604-606. doi: 10.1038/nsmb.3413. Epub 2017 May 22.

In mice, the pathway involving PIWI and PIWI-interacting RNA (PIWI-piRNA) is essential to re-establish transposon silencing during male-germline reprogramming. The cytoplasmic PIWI protein MILI mediates piRNA-guided transposon RNA cleavage as well as piRNA amplification. MIWI2's binding to piRNA and its nuclear localization are proposed to be dependent upon MILI function. Here, we demonstrate the existence of a piRNA biogenesis pathway that sustains partial MIWI2 function and reprogramming activity in the absence of MILI.

在小鼠中，涉及PIWI和PIWI相互作用RNA（PIWI-piRNA）的途径对于在雄性生殖系重编程过程中重新建立转座子沉默至关重要。细胞质PIWI蛋白MILI介导piRNA引导的转座子RNA切割以及piRNA扩增。MIWI2与piRNA的结合及其核定位被认为依赖于MILI的功能。在这里，我们证明了在没有MILI的情况下，存在一种维持部分MIWI2功能和重编程活性的piRNA生物发生途径。