期刊
JOURNAL OF CELL SCIENCE
卷 132, 期 8, 页码 -出版社
COMPANY BIOLOGISTS LTD
DOI: 10.1242/jcs.226258
关键词
Cytosolic translation; Mitochondrial stress; Reactive oxygen species; Redox switches
类别
资金
- 'Regenerative Mechanisms for Health' project [MAB/2017/2]
- European Union under the European Regional Development Fund [000263]
- National Science Centre [2015/18/A/NZ1/00025, 2015/19/B/NZ1/03444]
- POLONEZ Fellowship of the National Science Centre in Poland [2016/23/P/NZ3/03730]
- European Union's Horizon 2020 research and innovation program under Marie Sklodowska-Curie grant [665778]
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.
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