Re-establishment of nuclear structure and chromatin organization after cell division is integral for genome regulation or development and is frequently altered during cancer progression. The mechanisms underlying chromatin expansion in daughter cells remain largely unclear. Here, we describe the transient formation of nuclear actin filaments (F-actin) during mitotic exit. These nuclear F-actin structures assemble in daughter cell nuclei and undergo dynamic reorganization to promote nuclear protrusions and volume expansion throughout early G1 of the cell cycle. Specific inhibition of this nuclear F-actin assembly impaired nuclear expansion and chromatin decondensation after mitosis and during early mouse embryonic development. Biochemical screening for mitotic nuclear F-actin interactors identified the actin-disassembling factor cofilin-1. Optogenetic regulation of cofilin-1 revealed its critical role for controlling timing, turnover and dynamics of F-actin assembly inside daughter cell nuclei. Our findings identify a cell-cycle-specific and spatiotemporally controlled form of nuclear F-actin that reorganizes the mammalian nucleus after mitosis.

中文翻译：

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有丝分裂出口处的核 F-肌动蛋白瞬时池控制着染色质组织。

细胞分裂后核结构和染色质组织的重建是基因组调控或发育不可或缺的一部分，并且在癌症进展过程中经常发生改变。子细胞染色质扩张的机制在很大程度上仍不清楚。在这里，我们描述了有丝分裂退出期间核肌动蛋白丝（F-肌动蛋白）的瞬时形成。这些核 F-肌动蛋白结构在子细胞核中组装并进行动态重组，以促进整个细胞周期早期 G1 的核突出和体积膨胀。这种核 F-肌动蛋白组装的特异性抑制会损害有丝分裂后和早期小鼠胚胎发育过程中的核扩张和染色质解凝。有丝分裂核 F-肌动蛋白相互作用因子的生化筛选鉴定出肌动蛋白分解因子 cofilin-1。cofilin-1 的光遗传学调控揭示了其在控制子细胞核内 F-肌动蛋白组装的时间、周转和动态方面的关键作用。我们的研究结果确定了一种细胞周期特异性且时空控制的核 F-肌动蛋白形式，它可以在有丝分裂后重组哺乳动物的细胞核。