Lineage-specific SoxR-mediated Regulation of an Endoribonuclease Protects Non-enteric Bacteria from Redox-active Compounds.
J Biol Chem, 2017/1/06;292(1):121-133.
Kim J[1], Park C[1], Imlay JA[2], Park W[3]
Affiliations
PMID: 27895125DOI: 10.1074/jbc.M116.757500
Impact factor: 5.486
Abstract
Bacteria use redox-sensitive transcription factors to coordinate responses to redox stress. The [2Fe-2S] cluster-containing transcription factor SoxR is particularly tuned to protect cells against redox-active compounds (RACs). In enteric bacteria, SoxR is paired with a second transcription factor, SoxS, that activates downstream effectors. However, SoxS is absent in non-enteric bacteria, raising questions as to how SoxR functions. Here, we first show that SoxR of Acinetobacter oleivorans displayed similar activation profiles in response to RACs as did its homolog from Escherichia coli but controlled a different set of target genes, including sinE, which encodes an endoribonuclease. Expression, gel mobility shift, and mutational analyses indicated that sinE is a direct target of SoxR. Redox potentials and permeability of RACs determined optimal sinE induction. Bioinformatics suggested that only a few γ- and β-proteobacteria might have SoxR-regulated sinE Purified SinE, in the presence of Mg2+ ions, degrades rRNAs, thus inhibiting protein synthesis. Similarly, pretreatment of cells with RACs demonstrated a role for SinE in promoting persistence in the presence of antibiotics that inhibit protein synthesis. Our data improve our understanding of the physiology of soil microorganisms by suggesting that both non-enteric SoxR and its target SinE play protective roles in the presence of RACs and antibiotics.
Keywords: Acinetobacter; Escherichia coli (E. coli); SoxR; antibiotics; bacteria; biofilm; endoribonuclease; oxidative stress; reactive oxygen species (ROS); transcriptional regulation
MeSH terms
Acinetobacter; Anti-Bacterial Agents; Bacterial Proteins; Cell Lineage; Endoribonucleases; Escherichia coli; Escherichia coli Proteins; Gene Expression Regulation, Bacterial; Gene Expression Regulation, Enzymologic; Iron-Sulfur Proteins; Oxidation-Reduction; Protein Biosynthesis; Trans-Activators; Transcription Factors; Transcription, Genetic
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