2.50
Hdl Handle:
http://hdl.handle.net/10033/620772
Title:
The luxS mutation causes loosely-bound biofilms in Shewanella oneidensis
Authors:
Bodor, Agnes M; Jänsch, Lothar; Wissing, Josef; Wagner-Döbler, Irene
Abstract:
Abstract Background The luxS gene in Shewanella oneidensis was shown to encode an autoinducer-2 (AI-2)-like molecule, the postulated universal bacterial signal, but the impaired biofilm growth of a luxS deficient mutant could not be restored by AI-2, indicating it might not have a signalling role in this organism. Findings Here, we provide further evidence regarding the metabolic role of a luxS mutation in S. oneidensis. We constructed a luxS mutant and compared its phenotype to a wild type control with respect to its ability to remove AI-2 from the medium, expression of secreted proteins and biofilm formation. We show that S. oneidensis has a cell-dependent mechanism by which AI-2 is depleted from the medium by uptake or degradation at the end of the exponential growth phase. As AI-2 depletion is equally active in the luxS mutant and thus does not require AI-2 as an inducer, it appears to be an unspecific mechanism suggesting that AI-2 for S. oneidensis is a metabolite which is imported under nutrient limitation. Secreted proteins were studied by iTraq labelling and liquid chromatography mass spectrometry (LC-MS) detection. Differences between wild type and mutant were small. Proteins related to flagellar and twitching motility were slightly up-regulated in the luxS mutant, in accordance with its loose biofilm structure. An enzyme related to cysteine metabolism was also up-regulated, probably compensating for the lack of the LuxS enzyme. The luxS mutant developed an undifferentiated, loosely-connected biofilm which covered the glass surface more homogenously than the wild type control, which formed compact aggregates with large voids in between. Conclusions The data confirm the role of the LuxS enzyme for biofilm growth in S. oneidensis and make it unlikely that AI-2 has a signalling role in this organism.
Citation:
BMC Research Notes. 2011 Jun 10;4(1):180
Issue Date:
10-Jun-2011
URI:
http://dx.doi.org/10.1186/1756-0500-4-180; http://hdl.handle.net/10033/620772
Type:
Journal Article
Appears in Collections:
collections of the research group microbial communication (KOM)

Full metadata record

DC FieldValue Language
dc.contributor.authorBodor, Agnes Men
dc.contributor.authorJänsch, Lotharen
dc.contributor.authorWissing, Josefen
dc.contributor.authorWagner-Döbler, Ireneen
dc.date.accessioned2017-01-27T10:20:46Z-
dc.date.available2017-01-27T10:20:46Z-
dc.date.issued2011-06-10en
dc.identifier.citationBMC Research Notes. 2011 Jun 10;4(1):180en
dc.identifier.urihttp://dx.doi.org/10.1186/1756-0500-4-180en
dc.identifier.urihttp://hdl.handle.net/10033/620772-
dc.description.abstractAbstract Background The luxS gene in Shewanella oneidensis was shown to encode an autoinducer-2 (AI-2)-like molecule, the postulated universal bacterial signal, but the impaired biofilm growth of a luxS deficient mutant could not be restored by AI-2, indicating it might not have a signalling role in this organism. Findings Here, we provide further evidence regarding the metabolic role of a luxS mutation in S. oneidensis. We constructed a luxS mutant and compared its phenotype to a wild type control with respect to its ability to remove AI-2 from the medium, expression of secreted proteins and biofilm formation. We show that S. oneidensis has a cell-dependent mechanism by which AI-2 is depleted from the medium by uptake or degradation at the end of the exponential growth phase. As AI-2 depletion is equally active in the luxS mutant and thus does not require AI-2 as an inducer, it appears to be an unspecific mechanism suggesting that AI-2 for S. oneidensis is a metabolite which is imported under nutrient limitation. Secreted proteins were studied by iTraq labelling and liquid chromatography mass spectrometry (LC-MS) detection. Differences between wild type and mutant were small. Proteins related to flagellar and twitching motility were slightly up-regulated in the luxS mutant, in accordance with its loose biofilm structure. An enzyme related to cysteine metabolism was also up-regulated, probably compensating for the lack of the LuxS enzyme. The luxS mutant developed an undifferentiated, loosely-connected biofilm which covered the glass surface more homogenously than the wild type control, which formed compact aggregates with large voids in between. Conclusions The data confirm the role of the LuxS enzyme for biofilm growth in S. oneidensis and make it unlikely that AI-2 has a signalling role in this organism.en
dc.titleThe luxS mutation causes loosely-bound biofilms in Shewanella oneidensisen
dc.typeJournal Articleen
dc.language.rfc3066enen
dc.rights.holderBodor et al; licensee BioMed Central Ltd.en
dc.date.updated2015-09-04T08:28:16Zen
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