Faculty of Science and Engineering, Cell Biology, Åbo Akademi University, Tykistökatu 6, 20520 Turku, Finland.
Turku Bioscience Centre, University of Turku and Åbo Akademi University, Tykistökatu 6, 20520 Turku, Finland.
J Cell Sci. 2019 Nov 1;132(21):jcs238402. doi: 10.1242/jcs.238402.
Cellular stress triggers reprogramming of transcription, which is required for the maintenance of homeostasis under adverse growth conditions. Stress-induced changes in transcription include induction of cyto-protective genes and repression of genes related to the regulation of the cell cycle, transcription and metabolism. Induction of transcription is mediated through the activation of stress-responsive transcription factors that facilitate the release of stalled RNA polymerase II and so allow for transcriptional elongation. Repression of transcription, in turn, involves components that retain RNA polymerase II in a paused state on gene promoters. Moreover, transcription during stress is regulated by a massive activation of enhancers and complex changes in chromatin organization. In this Review, we highlight the latest research regarding the molecular mechanisms of transcriptional reprogramming upon stress in the context of specific proteotoxic stress responses, including the heat-shock response, unfolded protein response, oxidative stress response and hypoxia response.
细胞应激会引发转录重编程，这对于在不利的生长条件下维持体内平衡是必需的。转录的应激诱导变化包括细胞保护基因的诱导和与细胞周期、转录和代谢调节相关基因的抑制。转录的诱导是通过应激反应转录因子的激活来介导的，这有助于释放停滞的 RNA 聚合酶 II，从而允许转录延伸。相反，转录的抑制涉及到将 RNA 聚合酶 II 保留在基因启动子上暂停状态的组件。此外，应激期间的转录受到增强子的大量激活和染色质组织的复杂变化的调节。在这篇综述中，我们强调了在特定的蛋白毒性应激反应（包括热休克反应、未折叠蛋白反应、氧化应激反应和缺氧反应）背景下，应激时转录重编程的分子机制的最新研究。
