Abstract
Escherichia coli and related enteric bacteria can survive under extreme acid stress condition at least for several hours. RpoS is a key factor for acid stress management in many enterobacteria. Although three rpoS-activating sRNAs, DsrA, RprA, and ArcZ, have been identified in E. coli, it remains unclear how these small RNA molecules participate in pathways leading to acid resistance (AR). Here, we showed that overexpression of ArcZ, DsrA, or RprA enhances AR in a RpoS-dependent manner. Mutant strains with deletion of any of three sRNA genes showed lowered AR, and deleting all three sRNA genes led to more severe defects in protecting against acid stress. Overexpression of any of the three sRNAs fully rescued the acid tolerance defects of the mutant strain lacking all three genes, suggesting that all three sRNAs perform the same function in activating RpoS required for AR. Notably, acid stress led to the induction of DsrA and RprA but not ArcZ.
Highlights
Most pathogenic or nonpathogenic enterobacteria grow optimally at a pH range 5–9, and are classified as neutrophilic bacteria
On the basis of these findings, we propose a model of acid stress response by rpoS-activating sRNAs (Fig. 9)
We showed that a shift of exponentially growing E. coli cells to pH 5.0 increases the expression of translational rpoS-lacZ fusions and induces DsrA and RprA
Summary
Most pathogenic or nonpathogenic enterobacteria grow optimally at a pH range 5–9, and are classified as neutrophilic bacteria. The glutamate-dependent AR2 and arginine-dependent AR3 systems include amino acid–dependent decarboxylase complexes comprising amino acid decarboxylases and countertransporters that exchange decarboxylation products for new extracellular amino acids. Another AR system relying on L-glutamine, GadC, and glutaminase that releases gaseous a 2013 The Authors. It is not difficult to speculate that these sRNAs would provide E. coli with AR by activating rpoS expression, but roles of these small RNA molecules in pathways leading to AR remain elusive due to the complexity of mechanisms of AR. Our data should aid in improving our current understanding of the acquisition mechanisms of AR by E. coli cells through rpoS-activating sRNAs
Sign-in/Register to view highlights & summary 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 callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
