Mutations, protein homeostasis, and epigenetic control of genome integrity.
Mutations, protein homeostasis, and epigenetic control of genome integrity.
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DOI：
10.1016/j.dnarep.2018.08.004
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发表时间：
2018-11
期刊：
影响因子：
3.8
通讯作者：
Jarosz DF
中科院分区：
文献类型：
--
作者：
Xie JL;Jarosz DF
从细菌到人类，古老的应激反应使生物体能够应对基因组和蛋白质组的损害。这些途径长期以来被视为基本上独立的反应。然而，最近来自多个领域的发现揭示了两者之间令人惊讶的联系。许多DNA损伤剂也靶向蛋白质，并且由DNA损伤诱导的诱变产生易于错误折叠、降解和聚集的变体蛋白质。同样地，最近的研究已经观察到p53介导的反应以及与维持基因组完整性相关的其他因素在响应错误折叠的蛋白质应激中的普遍参与。也许最值得注意的是，现在已经在调节DNA损伤反应的多种蛋白质中观察到蛋白质聚集和自组装。癌症和神经退行性疾病模型突出了这些联系的重要性，其中受损的DNA修复机制导致蛋白质质量控制的严重缺陷，反之亦然。
From bacteria to humans, ancient stress responses enable organisms to contend with damage to both the genome and the proteome. These pathways have long been viewed as fundamentally separate responses. Yet recent discoveries from multiple fields have revealed surprising links between the two. Many DNA-damaging agents also target proteins, and mutagenesis induced by DNA damage produces variant proteins that are prone to misfolding, degradation, and aggregation. Likewise, recent studies have observed pervasive engagement of a p53-mediated response, and other factors linked to maintenance of genomic integrity, in response to misfolded protein stress. Perhaps most remarkably, protein aggregation and self-assembly has now been observed in multiple proteins that regulate the DNA damage response. The importance of these connections is highlighted by disease models of both cancer and neurodegeneration, in which compromised DNA repair machinery leads to profound defects in protein quality control, and vice versa.
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