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ATM mediated phosphorylation of CHD4 contributes to genome maintenance

机译：ATM介导的CHD4磷酸化有助于基因组维护

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Background In order to maintain cellular viability and genetic integrity cells must respond quickly following the induction of cytotoxic double strand DNA breaks (DSB). This response requires a number of processes including stabilisation of the DSB, signalling of the break and repair. It is becoming increasingly apparent that one key step in this process is chromatin remodelling. Results Here we describe the chromodomain helicase DNA-binding protein (CHD4) as a target of ATM kinase. We show that ionising radiation (IR)-induced phosphorylation of CHD4 affects its intranuclear organization resulting in increased chromatin binding/retention. We also show assembly of phosphorylated CHD4 foci at sites of DNA damage, which might be required to fulfil its function in the regulation of DNA repair. Consistent with this, cells overexpressing a phospho-mutant version of CHD4 that cannot be phosphorylated by ATM fail to show enhanced chromatin retention after DSBs and display high rates of spontaneous damage. Conclusion These results provide insight into how CHD4 phosphorylation might be required to remodel chromatin around DNA breaks allowing efficient DNA repair to occur.
机译：背景技术为了维持细胞活力和遗传完整性，细胞必须在诱导细胞毒性双链DNA断裂（DSB）后迅速作出反应。该响应需要许多过程，包括稳定DSB，发出中断信号和修复信号。越来越明显的是，该过程中的一个关键步骤是染色质重塑。结果在这里，我们描述了作为ATM激酶目标的染色体域解旋酶DNA结合蛋白（CHD4）。我们显示电离辐射（IR）诱导的CHD4磷酸化影响其核内组织，导致染色质结合/保留增加。我们还显示了在DNA损伤部位磷酸化CHD4病灶的组装，这可能是履行其在DNA修复调控中所必需的。与此相一致的是，过表达CHD4的磷酸突变型但不能被ATM磷酸化的细胞在DSB后不能显示出增强的染色质保留能力，并且显示出很高的自发损伤率。结论这些结果为深入了解如何可能需要CHD4磷酸化以重塑DNA断裂周围的染色质提供了有效的DNA修复方法。

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