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Human RAD51 paralogue SWSAP1 fosters RAD51 filament by regulating the anti-recombinase FIGNL1 AAA+ ATPase.
Nature Communications ( IF 14.7 ) Pub Date : 2019-03-29 , DOI: 10.1038/s41467-019-09190-1 Kenichiro Matsuzaki 1 , Shizuka Kondo 1, 2 , Tatsuya Ishikawa 1, 2 , Akira Shinohara 1
Nature Communications ( IF 14.7 ) Pub Date : 2019-03-29 , DOI: 10.1038/s41467-019-09190-1 Kenichiro Matsuzaki 1 , Shizuka Kondo 1, 2 , Tatsuya Ishikawa 1, 2 , Akira Shinohara 1
Affiliation
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RAD51 assembly on single-stranded (ss)DNAs is a crucial step in the homology-dependent repair of DNA damage for genomic stability. The formation of the RAD51 filament is promoted by various RAD51-interacting proteins including RAD51 paralogues. However, the mechanisms underlying the differential control of RAD51-filament dynamics by these factors remain largely unknown. Here, we report a role for the human RAD51 paralogue, SWSAP1, as a novel regulator of RAD51 assembly. Swsap1-deficient cells show defects in DNA damage-induced RAD51 assembly during both mitosis and meiosis. Defective RAD51 assembly in SWSAP1-depleted cells is suppressed by the depletion of FIGNL1, which binds to RAD51 as well as SWSAP1. Purified FIGNL1 promotes the dissociation of RAD51 from ssDNAs. The dismantling activity of FIGNL1 does not require its ATPase but depends on RAD51-binding. Purified SWSAP1 inhibits the RAD51-dismantling activity of FIGNL1. Taken together, our data suggest that SWSAP1 protects RAD51 filaments by antagonizing the anti-recombinase, FIGNL1.
中文翻译：
人类RAD51旁系同源物SWSAP1通过调节抗重组酶FIGNL1 AAA + ATPase来培育RAD51细丝。
RAD51在单链（ss）DNA上的组装是DNA损伤的同源性依赖性修复对基因组稳定性的关键步骤。包括RAD51旁系同源物在内的各种RAD51相互作用蛋白可促进RAD51细丝的形成。但是，通过这些因素对RAD51丝动力学进行差异控制的基本机制仍然未知。在这里，我们报告人类RAD51旁系SWSW1作为RAD51装配的新型调节剂的作用。Swsap1缺陷细胞在有丝分裂和减数分裂过程中都显示出DNA损伤诱导的RAD51装配中的缺陷。耗尽SWSAP1的细胞中RAD51的组装缺陷被FIGNL1的耗尽所抑制，FIGNL1的耗尽与RAD51以及SWSAP1结合。纯化的FIGNL1促进RAD51从ssDNA的解离。FIGNL1的拆卸活性不需要其ATPase，而取决于RAD51的结合。纯化的SWSAP1抑制FIGNL1的RAD51拆卸活性。两者合计，我们的数据表明SWSAP1通过拮抗抗重组酶FIGNL1保护RAD51细丝。
更新日期：2019-03-29
中文翻译：
人类RAD51旁系同源物SWSAP1通过调节抗重组酶FIGNL1 AAA + ATPase来培育RAD51细丝。
RAD51在单链（ss）DNA上的组装是DNA损伤的同源性依赖性修复对基因组稳定性的关键步骤。包括RAD51旁系同源物在内的各种RAD51相互作用蛋白可促进RAD51细丝的形成。但是，通过这些因素对RAD51丝动力学进行差异控制的基本机制仍然未知。在这里，我们报告人类RAD51旁系SWSW1作为RAD51装配的新型调节剂的作用。Swsap1缺陷细胞在有丝分裂和减数分裂过程中都显示出DNA损伤诱导的RAD51装配中的缺陷。耗尽SWSAP1的细胞中RAD51的组装缺陷被FIGNL1的耗尽所抑制，FIGNL1的耗尽与RAD51以及SWSAP1结合。纯化的FIGNL1促进RAD51从ssDNA的解离。FIGNL1的拆卸活性不需要其ATPase，而取决于RAD51的结合。纯化的SWSAP1抑制FIGNL1的RAD51拆卸活性。两者合计，我们的数据表明SWSAP1通过拮抗抗重组酶FIGNL1保护RAD51细丝。
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