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Journal of Bacteriology, February 2008, p. 1045-1053, Vol. 190, No. 3
0021-9193/08/$08.00+0 doi:10.1128/JB.01472-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Hai-Bao Zhang,1,
Jin-Ling Xu,1
Qiongguang Liu,2
Zide Jiang,2 and
Lian-Hui Zhang1*
Institute of Molecular and Cell Biology, 61 Biopolis Drive, Singapore 138673,1 Department of Plant Pathology, South China Agricultural University, Guangzhou 510642, People's Republic of China2
Received 12 September 2007/ Accepted 20 November 2007
Erwinia chrysanthemi pv. zeae is one of the Erwinia chrysanthemi pathovars that infects on both dicotyledons and monocotyledons. However, little is known about the molecular basis and regulatory mechanisms of its virulence. By using a transposon mutagenesis approach, we cloned the genes coding for an E. chrysanthemi pv. zeae synthase of acyl-homoserine lactone (AHL) quorum-sensing signals (expIEcz) and a cognate response regulator (expREcz). Chromatography analysis showed that expIEcz encoded production of the AHL signal N-(3-oxo-hexanoyl)-homoserine lactone (OHHL). Null mutation of expIEcz in the E. chrysanthemi pv. zeae strain EC1 abolished AHL production, increased bacterial swimming and swarming motility, disabled formation of multicell aggregates, and attenuated virulence of the pathogen on potato tubers. The mutation also marginally reduced the inhibitory activity of E. chrysanthemi pv. zeae on rice seed germination. The mutant phenotypes were rescued by either exogenous addition of AHL signal or in trans expression of expIEcz. These data demonstrate that the AHL-type QS signal plays an essential role in modulation of E. chrysanthemi pv. zeae cell motility and the ability to form multicell aggregates and is involved in regulation of bacterial virulence.
Published ahead of print on 14 December 2007.
M. B. B. M. Hussain and H.-B. Zhang contributed equally to this work.
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