Regulation of Burkholderia cenocepacia biofilm formation by RpoN and the c-di-GMP effector BerB.
dc.contributor.author | Fazli, Mustafa | |
dc.contributor.author | Rybtke, Morten | |
dc.contributor.author | Steiner, Elisabeth | |
dc.contributor.author | Weidel, Elisabeth | |
dc.contributor.author | Berthelsen, Jens | |
dc.contributor.author | Groizeleau, Julie | |
dc.contributor.author | Bin, Wu | |
dc.contributor.author | Zhi, Boo Zhao | |
dc.contributor.author | Yaming, Zhang | |
dc.contributor.author | Kaever, Volkhard | |
dc.contributor.author | Givskov, Michael | |
dc.contributor.author | Hartmann, Rolf W. | |
dc.contributor.author | Eberl, Leo | |
dc.contributor.author | Tolker-Nielsen, Tim | |
dc.date.accessioned | 2017-05-12T14:47:05Z | |
dc.date.available | 2017-05-12T14:47:05Z | |
dc.date.issued | 2017-04-16 | |
dc.identifier.citation | Regulation of Burkholderia cenocepacia biofilm formation by RpoN and the c-di-GMP effector BerB. 2017 Microbiologyopen | en |
dc.identifier.issn | 2045-8827 | |
dc.identifier.pmid | 28419759 | |
dc.identifier.doi | 10.1002/mbo3.480 | |
dc.identifier.uri | http://hdl.handle.net/10033/620917 | |
dc.description.abstract | Knowledge about the molecular mechanisms that are involved in the regulation of biofilm formation is essential for the development of biofilm-control measures. It is well established that the nucleotide second messenger cyclic diguanosine monophosphate (c-di-GMP) is a positive regulator of biofilm formation in many bacteria, but more knowledge about c-di-GMP effectors is needed. We provide evidence that c-di-GMP, the alternative sigma factor RpoN (σ54), and the enhancer-binding protein BerB play a role in biofilm formation of Burkholderia cenocepacia by regulating the production of a biofilm-stabilizing exopolysaccharide. Our findings suggest that BerB binds c-di-GMP, and activates RpoN-dependent transcription of the berA gene coding for a c-di-GMP-responsive transcriptional regulator. An increased level of the BerA protein in turn induces the production of biofilm-stabilizing exopolysaccharide in response to high c-di-GMP levels. Our findings imply that the production of biofilm exopolysaccharide in B. cenocepacia is regulated through a cascade involving two consecutive transcription events that are both activated by c-di-GMP. This type of regulation may allow tight control of the expenditure of cellular resources. | |
dc.language.iso | en | en |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-sa/4.0/ | * |
dc.title | Regulation of Burkholderia cenocepacia biofilm formation by RpoN and the c-di-GMP effector BerB. | en |
dc.type | Article | en |
dc.contributor.department | Helmholtz-Institut für Pharmazeutische Forschung Saarland, Universitätscampus E8.1, 66123 Saarbrücken, Germany. | en |
dc.identifier.journal | MicrobiologyOpen | en |
refterms.dateFOA | 2018-06-12T23:13:31Z | |
html.description.abstract | Knowledge about the molecular mechanisms that are involved in the regulation of biofilm formation is essential for the development of biofilm-control measures. It is well established that the nucleotide second messenger cyclic diguanosine monophosphate (c-di-GMP) is a positive regulator of biofilm formation in many bacteria, but more knowledge about c-di-GMP effectors is needed. We provide evidence that c-di-GMP, the alternative sigma factor RpoN (σ54), and the enhancer-binding protein BerB play a role in biofilm formation of Burkholderia cenocepacia by regulating the production of a biofilm-stabilizing exopolysaccharide. Our findings suggest that BerB binds c-di-GMP, and activates RpoN-dependent transcription of the berA gene coding for a c-di-GMP-responsive transcriptional regulator. An increased level of the BerA protein in turn induces the production of biofilm-stabilizing exopolysaccharide in response to high c-di-GMP levels. Our findings imply that the production of biofilm exopolysaccharide in B. cenocepacia is regulated through a cascade involving two consecutive transcription events that are both activated by c-di-GMP. This type of regulation may allow tight control of the expenditure of cellular resources. |