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Applied and Environmental Microbiology, March 2009, p. 1301-1307, Vol. 75, No. 5
0099-2240/09/$08.00+0 doi:10.1128/AEM.01393-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.
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Department of Geosciences, Virginia Polytechnic Institute and State University, Blacksburg, Virginia 24061,1 Biosciences Division, Oak Ridge National Laboratory, Oak Ridge, Tennessee 37831,2 Bioinformatics Research Center, North Carolina State University, Raleigh, North Carolina 27606,3 Department of Microbiology, Montana State University, Bozeman, Montana 59717,4 Department of Biological Sciences, Virginia Polytechnic Institute and State University, Blacksburg, Virginia 240615
Received 21 June 2008/ Accepted 28 December 2008
The role of LuxS in Shewanella oneidensis MR-1 has been examined by transcriptomic profiling, biochemical, and physiological experiments. The results indicate that a mutation in luxS alters biofilm development, not by altering quorum-sensing abilities but by disrupting the activated methyl cycle (AMC). The S. oneidensis wild type can produce a luminescence response in the AI-2 reporter strain Vibrio harveyi MM32. This luminescence response is abolished upon the deletion of luxS. The deletion of luxS also alters biofilm formations in static and flowthrough conditions. Genetic complementation restores the mutant biofilm defect, but the addition of synthetic AI-2 has no effect. These results suggest that AI-2 is not used as a quorum-sensing signal to regulate biofilm development in S. oneidensis. Growth on various sulfur sources was examined because of the involvement of LuxS in the AMC. A mutation in luxS produced a reduced ability to grow with methionine as the sole sulfur source. Methionine is a key metabolite used in the AMC to produce a methyl source in the cell and to recycle homocysteine. These data suggest that LuxS is important to metabolizing methionine and the AMC in S. oneidensis.
Published ahead of print on 5 January 2009.
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