JB
Home Help [Feedback] [For Subscribers] [Archive] [Search] --
JB Accepts, published online ahead of print on 30 March 2007
This Article
Right arrow Full Text (PDF)
Right arrow Other Versions of this Article:
JB.01510-06v1
189/11/4094    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
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 arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kim, Y.-K.
Right arrow Articles by McCarter, L. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kim, Y.-K.
Right arrow Articles by McCarter, L. L.

 Previous Article  |  Next Article 

J. Bacteriol. doi:10.1128/JB.01510-06
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

ScrG, a GGDEF-EAL protein, participates in regulating swarming and sticking in Vibrio parahaemolyticus

Yun-Kyeong Kim and Linda L. McCarter*

Department of Microbiology The University of Iowa Iowa City, Iowa 52242

* To whom correspondence should be addressed. Email: linda-mccarter{at}uiowa.edu.


   Abstract

In this work, we describe a new gene controlling lateral flagellar gene expression. The gene encodes ScrG, a protein containing GGDEF and EAL domains. This is the second GGDEF-EAL encoding locus determined to be involved in the regulation of swarming: the first was previously characterized and named scrABC (swarming and capsular polysaccharide regulation). GGDEF and EAL domain containing proteins participate in the synthesis and degradation of the nucleotide signal c-di-GMP in many bacteria. Overexpression of scrG was sufficient to induce lateral flagellar gene expression in liquid, decrease biofilm formation, decrease cps gene expression, and suppress the {Delta}scrABC phenotype. Removal of its EAL domain reversed ScrG activity, converting ScrG to an inhibitor of swarming and activator of cps expression. Overexpression of scrG decreased the intensity of a 32P-labeled nucleotide spot co-migrating with c-di-GMP standard, whereas overexpression of scrG{Delta}EAL enhanced the intensity of the spot. Mutants with defects in scrG showed altered swarming, lateral flagellin production and colony morphology (but not swimming motility); furthermore, mutation of two GGDEF-EAL encoding loci (scrG and scrABC) produced cumulative effects on swarming, lateral flagellar gene expression, lateral flagellin production and colony morphology. Mutant analysis supports the assignment of the primary in vivo activity of ScrG as being to act as a phosphodiesterase. The data are consistent with a model in which multiple GGDEF-EAL proteins can influence the cellular nucleotide pool: a low concentration of c-di-GMP favors surface mobility whereas high levels of this nucleotide promote a more adhesive cell type of V. parahaemolyticus.




This article has been cited by other articles:




Home Help [Feedback] [For Subscribers] [Archive] [Search] --
Appl. Environ. Microbiol. Infect. Immun. Eukaryot. Cell
Mol. Cell. Biol. J. Virol. Microbiol. Mol. Biol. Rev.
ALL ASM JOURNALS

Copyright © 2007 by the American Society for Microbiology. All rights reserved.