Post-transcriptional regulation during stress

Abstract

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.

Destructive effects of UVC radiation on Drosophila melanogaster: Mortality, fertility, mutations, and molecular mechanisms

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The effects of selenium on the translation efficiency of selenoproteins Gpx1, Gpx4, and Txnrd1 in oxLDL-induced EA.hy926 cells

“…TXNRD1 expression was mainly regulated at the translational level. This may be related to the fact that cells are subjected to post-transcriptional regulation during oxidative stress, and that regulation at the translational stage saves time and allows for a faster response to oxidative stress [59] .…”

Cellular clarity: a logistic regression approach to identify root epidermal regulators of iron deficiency response

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