BMC Genomics Research article Small noncoding RNA GcvB is a novel regulator of acid resistance in Escherichia coli Ye Jin1, Rory M Watt2, Antoine Danchin3 and Jian-dong Huang*1 BioMed Central Open Access Address: 1Department of Biochemistry, Li Ka Shing Faculty of Medicine, University of Hong Kong, Pok Fu Lam, Hong Kong SAR, PR China, 2Oral Biosciences, Faculty of Dentistry, University of Hong Kong, Pok Fu Lam, Hong Kong SAR, PR China and 3Genetics of Bacterial Genomes, CNRS URA2171, Institut Pasteur, 28, rue du Docteur Roux, Paris Cedex 15, 75724, France Email: Ye Jin - yejin@hkucc.hku.hk; Rory M Watt - rmwatt@hku.hk; Antoine Danchin - antoine.danchin@normalesup.org; Jian- dong Huang* - jdhuang@hkucc.hku.hk * Corresponding author Published: 20 April 2009 BMC Genomics 2009, 10:165 doi:10.1186/1471-2164-10-165 This article is available from: http://www.biomedcentral.com/1471-2164/10/165 Received: 26 January 2009 Accepted: 20 April 2009 © 2009 Jin et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Background: The low pH environment of the human stomach is lethal for most microorganisms; but not Escherichia coli, which can tolerate extreme acid stress. Acid resistance in E. coli is hierarchically controlled by numerous regulators among which are small noncoding RNAs (sncRNA). Results: In this study, we individually deleted seventy-nine sncRNA genes from the E. coli K12- MG1655 chromosome, and established a single-sncRNA gene knockout library. By systematically screening the sncRNA mutant library, we show that the sncRNA GcvB is a novel regulator of acid resistance in E. coli. We demonstrate that GcvB enhances the ability of E. coli to survive low pH by upregulating the levels of the alternate sigma factor RpoS. Conclusion: GcvB positively regulates acid resistance by affecting RpoS expression. These data advance our understanding of the sncRNA regulatory network involved in modulating acid resistance in E. coli. Background The ability to survive the extremely low pH environment present within the stomach (pH values < 2.5) is essential for colonization of the intestine by commensals and for the pathogenesis of enteric bacteria. Three distinct acid resistance (AR) systems are responsible for protecting bac- terial cells from acid shock [1-3]. AR system 1 is a glucose- repressed system and does not require any external amino acids to function at low pH [1]. Unidentified components of this system are controlled by the alternate sigma factor RpoS, with the underlying mechanism remaining unclear [1]. In contrast, AR systems 2 and 3 provide AR by con- suming intracellular protons via the glutamate (AR2) and arginine (AR3) decarboxylation reactions [2,3]. AR2 is the most efficient AR system. It involves two isozymes of glutamate decarboxylase, encoded by genes gadA and gadB, and a membrane-associated antiporter (GadC) that exchanges external glutamate for the intracellular decar- boxylation product γ-aminobutyric acid (GABA) [2]. AR2 is hierarchically regulated by multiple regulators, which include small noncoding RNAs (sncRNA) DsrA and possibly GadY. DsrA activates the expression of rpoS [4] and several AR genes including hdeAB, gadAX, and gadBC [5]. GadY, whose effects on AR have yet to be determined, controls the synthesis of GadX and GadW, which are reg- Page 1 of 7 (page number not for citation purposes)