Heterochromatin mainly comprises repeated DNA sequences that are prone to ectopic recombination. In Drosophila cells, ‘safe’ repair of heterochromatic double-strand breaks by homologous recombination relies on the relocalization of repair sites to the nuclear periphery before strand invasion. The mechanisms responsible for this movement were unknown. Here we show that relocalization occurs by directed motion along nuclear actin filaments assembled at repair sites by the Arp2/3 complex. Relocalization requires nuclear myosins associated with the heterochromatin repair complex Smc5/6 and the myosin activator Unc45, which is recruited to repair sites by Smc5/6. ARP2/3, actin nucleation and myosins also relocalize heterochromatic double-strand breaks in mouse cells. Defects in this pathway result in impaired heterochromatin repair and chromosome rearrangements. These findings identify de novo nuclear actin filaments and myosins as effectors of chromatin dynamics for heterochromatin repair and stability in multicellular eukaryotes.Relocalization of heterochromatic double-strand breaks to the nuclear periphery in Drosophila cells occurs via directed motions driven by nuclear actin filaments and myosins activated by the Smc5/6 complex.

中文翻译：

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核 F-肌动蛋白和肌球蛋白驱动异染色质断裂的重新定位

异染色质主要由容易发生异位重组的重复DNA序列组成。在果蝇细胞中，通过同源重组对异染色质双链断裂的“安全”修复依赖于链入侵之前修复位点重新定位到核外围。造成这种运动的机制尚不清楚。在这里，我们表明，重新定位是通过沿着由 Arp2/3 复合物在修复位点组装的核肌动蛋白丝进行定向运动而发生的。重新定位需要与异染色质修复复合物 Smc5/6 和肌球蛋白激活剂 Unc45 相关的核肌球蛋白，后者被 Smc5/6 招募到修复位点。ARP2/3、肌动蛋白成核和肌球蛋白也会重新定位小鼠细胞中的异染色质双链断裂。该途径的缺陷会导致异染色质修复和染色体重排受损。这些发现确定了从头核肌动蛋白丝和肌球蛋白是多细胞真核生物异染色质修复和稳定性染色质动力学的效应器。果蝇细胞中异染色质双链断裂的重新定位是通过由核肌动蛋白丝和肌球蛋白激活驱动的定向运动而发生的。由 Smc5/6 复合物产生。