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首页> 美国卫生研究院文献>Oncotarget >Human CRL4DDB2 ubiquitin ligase preferentially regulates post-repair chromatin restoration of H3K56Ac through recruitment of histone chaperon CAF-1
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Human CRL4DDB2 ubiquitin ligase preferentially regulates post-repair chromatin restoration of H3K56Ac through recruitment of histone chaperon CAF-1

机译：人类CRL4DDB2泛素连接酶通过募集组蛋白伴侣CAF-1优先调节H3K56Ac的修复后染色质恢复

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Acetylated histone H3 lysine 56 (H3K56Ac) diminishes in response to DNA damage but is restored following DNA repair. Here, we report that CRL4DDB2 ubiquitin ligase preferentially regulates post-repair chromatin restoration of H3K56Ac through recruitment of histone chaperon CAF-1. We show that H3K56Ac accumulates at DNA damage sites. The restoration of H3K56Ac but not H3K27Ac, H3K18Ac and H3K14Ac depends on CAF-1 function, whereas all these acetylations are mediated by CBP/p300. The CRL4DDB2 components, DDB1, DDB2 and CUL4A, are also required for maintaining the H3K56Ac and H3K9Ac level in chromatin, and for restoring H3K56Ac following induction of DNA photolesions and strand breaks. Depletion of CUL4A decreases the recruitment of CAF-1 p60 and p150 to ultraviolet radiation- and phleomycin-induced DNA damage. Neddylation inhibition renders CRL4DDB2 inactive, decreases H3K56Ac level, diminishes CAF-1 recruitment and prevents H3K56Ac restoration. Mutation in the PIP box of DDB2 compromises its capability to elevate the H3K56Ac level but does not affect XPC ubiquitination. These results demonstrated a function of CRL4DDB2 in differential regulation of histone acetylation in response to DNA damage, suggesting a novel role of CRL4DDB2 in repair-driven chromatin assembly.
机译：乙酰化的组蛋白H3赖氨酸56（H3K56Ac）响应DNA损伤而减少，但在DNA修复后得以恢复。在此，我们报道CRL4 DDB2 泛素连接酶通过募集组蛋白伴侣CAF-1优先调节H3K56Ac的修复后染色质恢复。我们显示H3K56Ac积累在DNA损伤部位。 H3K56Ac而不是H3K27Ac，H3K18Ac和H3K14Ac的恢复取决于CAF-1功能，而所有这些乙酰化作用均由CBP / p300介导。还需要CRL4 DDB2 组件DDB1，DDB2和CUL4A来维持染色质中的H3K56Ac和H3K9Ac水平，并在诱导DNA光损伤和链断裂后恢复H3K56Ac。 CUL4A的消耗减少了CAF-1 p60和p150对紫外线和光霉素诱导的DNA损伤的募集。 Neddylation抑制使CRL4 DDB2 失活，降低H3K56Ac水平，减少CAF-1募集并阻止H3K56Ac恢复。 DDB2的PIP框中的突变会损害其提高H3K56Ac水平的能力，但不会影响XPC泛素化。这些结果证明了CRL4 DDB2 在响应DNA损伤的组蛋白乙酰化的差异调节中的功能，表明CRL4 DDB2 在修复驱动的染色质组装中具有新的作用。

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