Abstract
Bacterial oxidative stress responses are generally controlled by transcription factors that modulate the synthesis of RNAs with the aid of some sRNAs that control the stability, and in some cases the translation, of specific mRNAs. Here, we report that oxidative stress additionally leads to inactivation of tRNAGly in Escherichia coli, inducing a series of physiological changes. The observed inactivation of tRNAGly correlated with altered efficiency of translation of Gly codons, suggesting a possible mechanism of translational control of gene expression under oxidative stress. Changes in translation also depended on the availability of glycine, revealing a mechanism whereby bacteria modulate the response to oxidative stress according to the prevailing metabolic state of the cells.
Highlights
Bacteria, like other organisms, need to adapt to environmental conditions that are constantly changing
Total transfer RNA (tRNA) was purified from E. coli K-12 MG1655 (Blattner et al, 1997) cells cultivated under control conditions or oxidative stress induced by addition of 1 mM paraquat or 2.5 mM H2O2
We demonstrate that oxidative stress induces specific alterations in the tRNAGly pools and concurrent changes in Gly codon translation rates
Summary
Like other organisms, need to adapt to environmental conditions that are constantly changing. Some of these conditions induce oxidative stress in bacteria due to either an increase in oxidants or a decrease in the ability of bacteria to defend against them. Oxidative stress induces some members from a bacterial community to enter a partially quiescent state known as “persistence” (Wu et al, 2012), where several primary metabolic pathways are repressed and stress responses are induced (Lewis, 2010; Cohen et al, 2013)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
