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Infection and Immunity, July 2005, p. 4127-4137, Vol. 73, No. 7
0019-9567/05/$08.00+0 doi:10.1128/IAI.73.7.4127-4137.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
Department of Biological Sciences, Faculty of Science, National University of Singapore, Singapore 117543, Republic of Singapore
Received 12 November 2004/ Returned for modification 22 January 2005/ Accepted 7 March 2005
Edwardsiella tarda is a gram-negative enteric pathogen that causes hemorrhagic septicemia in fish and gastro- and extraintestinal infections in humans. A type III secretion system (TTSS) and a putative secretion system (EVP) have been found to play important roles in E. tarda pathogenesis. Our previous studies suggested that the TTSS and EVP gene clusters were regulated by a two-component system of EsrA-EsrB. In the present study, we characterized another regulator, EsrC, which showed significant sequence similarity to the AraC family of transcriptional regulators. Mutants with in-frame deletions of esrC increased the 50% lethal doses in blue gourami fish, reduced extracellular protein production, and failed to aggregate. Complementation of esrC restored these three phenotypes. Two-dimensional gel electrophoresis showed that EsrC regulated the expression of secreted proteins encoded by the TTSS (such as EseB and EseD) and EVP (EvpC) gene clusters. The expression of esrC required a functional two-component system of EsrA-EsrB. EsrC in turn regulated the expression of selected genes encoded in TTSS (such as the transcriptional unit of orf29and orf30, but not esaC) and genes encoded in the EVP gene cluster. The present study sheds light on the regulation of these two key virulence-associated secretion systems and provides greater insight into the pathogenic mechanisms of this bacterium.
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