Post-transcriptional regulation during stress

To remain competitive, cells exposed to stress of varying duration, rapidity of onset, and intensity, have to balance their expenditure on growth and proliferation versus stress protection. To a large degree dependent on the time scale of stress exposure, the different levels of gene expression control: transcriptional, post-transcriptional, and post-translational, will be engaged in stress responses. The post-transcriptional level is appropriate for minute-scale responses to transient stress, and for recovery upon return to normal conditions. The turnover rate, translational activity, covalent modifications, and subcellular localisation of RNA species are regulated under stress by multiple cellular pathways. The interplay between these pathways is required to achieve the appropriate signalling intensity and prevent undue triggering of stress-activated pathways at low stress levels, avoid overshoot, and down-regulate the response in a timely fashion. As much of our understanding of post-transcriptional regulation has been gained in yeast, this review is written with a yeast bias, but attempts to generalise to other eukaryotes. It summarises aspects of how post-transcriptional events in eukaryotes mitigate short-term environmental stresses, and how different pathways interact to optimise the stress response under shifting external conditions. The authors review how different regulatory pathways on the RNA level interact to allow eukaryotic cells to survive and proliferate under stress conditions.

Automated summary

To remain competitive, cells need to balance growth and proliferation with stress protection. Different levels of gene expression control are engaged in stress responses depending on the time scale of stress exposure. Post-transcriptional control is appropriate for minute-scale responses to transient stress and recovery. It regulates the turnover rate, translational activity, covalent modifications, and subcellular localization of RNA species through multiple cellular pathways to achieve appropriate signaling intensity, avoid undue triggering of stress-activated pathways, and timely down-regulate the response.