A Suppressor Mutation That Creates a Faster and More Robust σE Envelope Stress Response.

TitleA Suppressor Mutation That Creates a Faster and More Robust σE Envelope Stress Response.
Publication TypeJournal Article
Year of Publication2016
AuthorsKonovalova, A, Schwalm, JA, Silhavy, TJ
JournalJ Bacteriol
Volume198
Issue17
Pagination2345-51
Date Published2016 09 01
ISSN1098-5530
KeywordsBacterial Outer Membrane Proteins, Cell Membrane, Escherichia coli, Gene Expression Regulation, Bacterial, Mutation, Protein Transport, Sigma Factor, Signal Transduction, Transcription Factors
Abstract

<p><b>UNLABELLED: </b>The σE envelope stress response is an essential signal transduction pathway which detects and removes mistargeted outer membrane (OM) β-barrel proteins (OMPs) in the periplasm of Escherichia coli It relies on σE, an alternative sigma factor encoded by the rpoE gene. Here we report a novel mutation, a nucleotide change of C to A in the third base of the second codon, which increases levels of σE (rpoE_S2R). The rpoE_S2R mutation does not lead to the induction of the stress response during normal growth but instead changes the dynamics of induction upon periplasmic stress, resulting in a faster and more robust response. This allows cells to adapt faster to the periplasmic stress, avoiding lethal accumulation of unfolded OMPs in the periplasm caused by severe defects in the OMP assembly pathway.</p><p><b>IMPORTANCE: </b>Survival of bacteria under conditions of external or internal stresses depends on timely induction of stress response signaling pathways to regulate expression of appropriate genes that function to maintain cellular homeostasis. Previous studies have shown that strong preinduction of envelope stress responses can allow bacteria to survive a number of lethal genetic perturbations. In our paper, we describe a unique mutation that enhances kinetics of the σE envelope stress response pathway rather than preinducing the response. This allows bacteria to quickly adapt to sudden and severe periplasmic stress.</p>

DOI10.1128/JB.00340-16
Alternate JournalJ. Bacteriol.
PubMed ID27325680
PubMed Central IDPMC4984553
Grant ListR35 GM118024 / GM / NIGMS NIH HHS / United States