Zhang Qiang, Bhattacharya Sudin, Pi Jingbo, Clewell Rebecca A, Carmichael Paul L, Andersen Melvin E
*Institute for Chemical Safety Sciences, The Hamner Institutes for Health Sciences, Research Triangle Park, North Carolina 27709; School of Public Health, China Medical University, Shenyang, China; and Unilever, Safety and Environmental Assurance Centre, Colworth Science Park, Sharnbrook, Bedfordshire, UK
*Institute for Chemical Safety Sciences, The Hamner Institutes for Health Sciences, Research Triangle Park, North Carolina 27709; School of Public Health, China Medical University, Shenyang, China; and Unilever, Safety and Environmental Assurance Centre, Colworth Science Park, Sharnbrook, Bedfordshire, UK.
Toxicol Sci. 2015 Oct;147(2):302-16. doi: 10.1093/toxsci/kfv130.
Although transcriptional induction of stress genes constitutes a major cellular defense program against a variety of stressors, posttranslational control directly regulating the activities of preexisting stress proteins provides a faster-acting alternative response. We propose that posttranslational control is a general adaptive mechanism operating in many stress pathways. Here with the aid of computational models, we first show that posttranslational control fulfills two roles: (1) handling small, transient stresses quickly and (2) stabilizing the negative feedback transcriptional network. We then review the posttranslational control pathways for major stress responses-oxidative stress, metal stress, hyperosmotic stress, DNA damage, heat shock, and hypoxia. Posttranslational regulation of stress protein activities occurs by reversible covalent modifications, allosteric or non-allosteric enzymatic regulations, and physically induced protein structural changes. Acting in feedback or feedforward networks, posttranslational control may establish a threshold level of cellular stress. Sub-threshold stresses are handled adequately by posttranslational control without invoking gene transcription. With supra-threshold stress levels, cellular homeostasis cannot be maintained and transcriptional induction of stress genes and other gene programs, eg, those regulating cell metabolism, proliferation, and apoptosis, takes place. The loss of homeostasis with consequent changes in cellular function may lead to adverse cellular outcomes. Overall, posttranslational and transcriptional control pathways constitute a stratified cellular defense system, handling stresses coherently across time and intensity. As cell-based assays become a focus for chemical testing anchored on toxicity pathways, examination of proteomic and metabolomic changes as a result of posttranslational control occurring in the absence of transcriptomic alterations deserves more attention.
尽管应激基因的转录诱导构成了细胞针对多种应激源的主要防御程序,但直接调节已有应激蛋白活性的翻译后控制提供了一种作用更快的替代反应。我们提出翻译后控制是一种在许多应激途径中起作用的普遍适应性机制。在此,借助计算模型,我们首先表明翻译后控制发挥两个作用:(1)快速应对小的、短暂的应激;(2)稳定负反馈转录网络。然后我们综述了主要应激反应——氧化应激、金属应激、高渗应激、DNA损伤、热休克和缺氧——的翻译后控制途径。应激蛋白活性的翻译后调节通过可逆共价修饰、别构或非别构酶促调节以及物理诱导的蛋白质结构变化来实现。在反馈或前馈网络中起作用时,翻译后控制可能会建立细胞应激的阈值水平。低于阈值的应激由翻译后控制充分应对,而无需启动基因转录。当应激水平超过阈值时,细胞稳态无法维持,应激基因和其他基因程序(例如调节细胞代谢、增殖和凋亡的程序)的转录诱导就会发生。稳态的丧失以及随之而来的细胞功能变化可能导致不良的细胞结果。总体而言,翻译后和转录控制途径构成了一个分层的细胞防御系统,能在时间和强度上连贯地应对应激。随着基于细胞的检测成为基于毒性途径的化学测试的重点,在不存在转录组改变的情况下,对翻译后控制导致的蛋白质组和代谢组变化的研究值得更多关注。