Centre of New Technologies, University of Warsaw, Banacha 2C, Warsaw 02-097, Poland
Department of Genetics, Institute of Biochemistry and Biophysics, Polish Academy of Sciences, Pawinskiego 5a, Warsaw 02-106, Poland.
J Cell Sci. 2019 Apr 26;132(8):jcs226258. doi: 10.1242/jcs.226258.
The production of newly synthesized proteins is vital for all cellular functions and is a determinant of cell growth and proliferation. The synthesis of polypeptide chains from mRNA molecules requires sophisticated machineries and mechanisms that need to be tightly regulated, and adjustable to current needs of the cell. Failures in the regulation of translation contribute to the loss of protein homeostasis, which can have deleterious effects on cellular function and organismal health. Unsurprisingly, the regulation of translation appears to be a crucial element in stress response mechanisms. This review provides an overview of mechanisms that modulate cytosolic protein synthesis upon cellular stress, with a focus on the attenuation of translation in response to mitochondrial stress. We then highlight links between mitochondrion-derived reactive oxygen species and the attenuation of reversible cytosolic translation through the oxidation of ribosomal proteins at their cysteine residues. We also discuss emerging concepts of how cellular mechanisms to stress are adapted, including the existence of alternative ribosomes and stress granules, and the regulation of co-translational import upon organelle stress.
新合成蛋白质的产生对所有细胞功能至关重要，是决定细胞生长和增殖的因素。从 mRNA 分子合成多肽链需要复杂的机器和机制，这些机制需要被严格调控，并能适应细胞当前的需求。翻译调控的失败导致蛋白质内稳态的丧失，这可能对细胞功能和生物体健康产生有害影响。毫不奇怪，翻译的调控似乎是应激反应机制的关键因素。本综述概述了细胞应激时调节细胞质蛋白合成的机制，重点介绍了线粒体应激时翻译的衰减。然后，我们强调了线粒体来源的活性氧与通过半胱氨酸残基氧化核糖体蛋白来衰减可逆细胞质翻译之间的联系。我们还讨论了细胞应激适应机制的一些新观点，包括替代核糖体和应激颗粒的存在，以及细胞器应激时共翻译导入的调控。
