Microbiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Microbiology 154 (2008), 2060-2069; DOI  10.1099/mic.0.2008/017343-0
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via CrossRef
Google Scholar
Right arrow Articles by Zhang, M.
Right arrow Articles by Sun, L.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Zhang, M.
Right arrow Articles by Sun, L.
Agricola
Right arrow Articles by Zhang, M.
Right arrow Articles by Sun, L.
Microbiology 154 (2008), 2060-2069; DOI  10.1099/mic.0.2008/017343-0
© 2008 Society for General Microbiology

Regulation of autoinducer 2 production and luxS expression in a pathogenic Edwardsiella tarda strain

Min Zhang1,2, Kun Sun1,2 and Li Sun1

1 Institute of Oceanology, Chinese Academy of Sciences, Qingdao 266071, PR China
2 Graduate University of the Chinese Academy of Sciences, Beijing 100049, PR China

Correspondence
Li Sun
lsun{at}ms.qdio.ac.cn

Edwardsiella tarda is a bacterial pathogen that can infect both humans and animals. TX1, an Ed. tarda strain isolated from diseased fish, was found to produce autoinducer 2 (AI-2)-like activity that was growth phase dependent and modulated by growth conditions. The gene coding for the AI-2 synthase was cloned from TX1 and designated luxSEt. LuxSEt was able to complement the AI-2 mutant phenotype of Escherichia coli strain DH5{alpha}. Expression of luxSEt correlated with AI-2 activity and was increased by glucose and decreased by elevated temperature. The effect of glucose was shown to be mediated through the cAMP-CRP complex, which repressed luxSEt expression. Overexpression of luxSEt enhanced AI-2 activity in TX1, whereas disruption of luxSEt expression by antisense RNA interference (i) reduced the level of AI-2 activity, (ii) impaired bacterial growth under various conditions, (iii) weakened the expression of genes associated with the type III secretion system and biofilm formation, and (iv) attenuated bacterial virulence. Addition of exogenous AI-2 was able to complement the deficiencies in the expression of TTSS genes and biofilm production but failed to rescue the growth defects. Our results (i) demonstrated that the AI-2 activity in TX1 is controlled at least in part at the level of luxSEt expression, which in turn is regulated by growth conditions, and that the temporal expression of luxSEt is essential for optimal bacterial infection and survival; and (ii) suggested the existence in Ed. tarda of a LuxS/AI-2-mediated signal transduction pathway that regulates the production of virulence-associated elements.


Abbreviations: AI-2, autoinducer 2; CRP, cAMP receptor protein; EMSA, electrophoretic mobility shift assay; i.p., intraperitoneally; QS, quorum sensing; RITT, rho-independent transcriptional terminator; TTSS, type III secretion system

The GenBank/EMBL/DDBJ accession number for the sequence of the luxSEt region is EU070919.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
INT J SYST EVOL MICROBIOL MICROBIOLOGY J GEN VIROL
J MED MICROBIOL ALL SGM JOURNALS
Copyright © 2008 Society for General Microbiology.