The piRNA pathway protects germline genomes from selfish genetic elements (e.g. transposons) through their transcript cleavage in the cytoplasm and/or their transcriptional silencing in the nucleus. Here, we describe a mechanism by which the nuclear and cytoplasmic arms of the piRNA pathway are linked. We find that during mitosis of Drosophila spermatogonia, nuclear Piwi interacts with nuage, the compartment that mediates the cytoplasmic arm of the piRNA pathway. At the end of mitosis, Piwi leaves nuage to return to the nucleus. Dissociation of Piwi from nuage occurs at the depolymerizing microtubules of the central spindle, mediated by a microtubule-depolymerizing kinesin, Klp10A. Depletion of klp10A delays the return of Piwi to the nucleus and affects piRNA production, suggesting the role of nuclear-cytoplasmic communication in piRNA biogenesis. We propose that cell cycle-dependent communication between the nuclear and cytoplasmic arms of the piRNA pathway may play a previously unappreciated role in piRNA regulation.

piRNA途径通过其在细胞质中的转录裂解和/或在细胞核中的转录沉默，保护种系基因组免受自私的遗传因素（例如转座子）的侵害。在这里，我们描述了一种机制，通过该机制piRNA途径的核和胞质臂相互连接。我们发现，在果蝇的精子细胞有丝分裂期间，核Piwi与nuage相互作用，nuage介导piRNA途径的胞质臂。在有丝分裂结束时，Piwi离开小核回到核。Piwi从纽结的解离发生在中心纺锤体的解聚微管上，由微管解聚驱动蛋白Klp10A介导。klp10A耗尽延缓了Piwi返回细胞核并影响piRNA的产生，提示核质间通讯在piRNA生物发生中的作用。我们提出，piRNA途径的核和胞质臂之间的细胞周期依赖性通信可能在piRNA调节中起着以前未被认识的作用。