| pubmed-article:16352847 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16352847 | lifeskim:mentions | umls-concept:C0014834 | lld:lifeskim |
| pubmed-article:16352847 | lifeskim:mentions | umls-concept:C1510470 | lld:lifeskim |
| pubmed-article:16352847 | lifeskim:mentions | umls-concept:C1325881 | lld:lifeskim |
| pubmed-article:16352847 | lifeskim:mentions | umls-concept:C2587213 | lld:lifeskim |
| pubmed-article:16352847 | lifeskim:mentions | umls-concept:C1704735 | lld:lifeskim |
| pubmed-article:16352847 | lifeskim:mentions | umls-concept:C0679622 | lld:lifeskim |
| pubmed-article:16352847 | lifeskim:mentions | umls-concept:C0205314 | lld:lifeskim |
| pubmed-article:16352847 | lifeskim:mentions | umls-concept:C0380349 | lld:lifeskim |
| pubmed-article:16352847 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:16352847 | pubmed:dateCreated | 2005-12-14 | lld:pubmed |
| pubmed-article:16352847 | pubmed:abstractText | The cross-species bacterial communication signal autoinducer 2 (AI-2), produced by the purified enzymes Pfs (nucleosidase) and LuxS (terminal synthase) from S-adenosylhomocysteine, directly increased Escherichia coli biofilm mass 30-fold. Continuous-flow cells coupled with confocal microscopy corroborated these results by showing the addition of AI-2 significantly increased both biofilm mass and thickness and reduced the interstitial space between microcolonies. As expected, the addition of AI-2 to cells which lack the ability to transport AI-2 (lsr null mutant) failed to stimulate biofilm formation. Since the addition of AI-2 increased cell motility through enhanced transcription of five motility genes, we propose that AI-2 stimulates biofilm formation and alters its architecture by stimulating flagellar motion and motility. It was also found that the uncharacterized protein B3022 regulates this AI-2-mediated motility and biofilm phenotype through the two-component motility regulatory system QseBC. Deletion of b3022 abolished motility, which was restored by expressing b3022 in trans. Deletion of b3022 also decreased biofilm formation significantly, relative to the wild-type strain in three media (46 to 74%) in 96-well plates, as well as decreased biomass (8-fold) and substratum coverage (19-fold) in continuous-flow cells with minimal medium (growth rate not altered and biofilm restored by expressing b3022 in trans). Deleting b3022 changed the wild-type biofilm architecture from a thick (54-mum) complex structure to one that contained only a few microcolonies. B3022 positively regulates expression of qseBC, flhD, fliA, and motA, since deleting b3022 decreased their transcription by 61-, 25-, 2.4-, and 18-fold, respectively. Transcriptome analysis also revealed that B3022 induces crl (26-fold) and flhCD (8- to 27-fold). Adding AI-2 (6.4 muM) increased biofilm formation of wild-type K-12 MG1655 but not that of the isogenic b3022, qseBC, fliA, and motA mutants. Adding AI-2 also increased motA transcription for the wild-type strain but did not stimulate motA transcription for the b3022 and qseB mutants. Together, these results indicate AI-2 induces biofilm formation in E. coli through B3022, which then regulates QseBC and motility; hence, b3022 has been renamed the motility quorum-sensing regulator gene (the mqsR gene). | lld:pubmed |
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| pubmed-article:16352847 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16352847 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16352847 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:16352847 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16352847 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:16352847 | pubmed:issn | 0021-9193 | lld:pubmed |
| pubmed-article:16352847 | pubmed:author | pubmed-author:WoodThomas... | lld:pubmed |
| pubmed-article:16352847 | pubmed:author | pubmed-author:BentleyWillia... | lld:pubmed |
| pubmed-article:16352847 | pubmed:author | pubmed-author:YangLiL | lld:pubmed |
| pubmed-article:16352847 | pubmed:author | pubmed-author:HashimotoYosh... | lld:pubmed |
| pubmed-article:16352847 | pubmed:author | pubmed-author:ZuoRongjunR | lld:pubmed |
| pubmed-article:16352847 | pubmed:author | pubmed-author:González... | lld:pubmed |
| pubmed-article:16352847 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16352847 | pubmed:volume | 188 | lld:pubmed |
| pubmed-article:16352847 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16352847 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16352847 | pubmed:pagination | 305-16 | lld:pubmed |
| pubmed-article:16352847 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
| pubmed-article:16352847 | pubmed:meshHeading | pubmed-meshheading:16352847... | lld:pubmed |
| pubmed-article:16352847 | pubmed:meshHeading | pubmed-meshheading:16352847... | lld:pubmed |
| pubmed-article:16352847 | pubmed:meshHeading | pubmed-meshheading:16352847... | lld:pubmed |
| pubmed-article:16352847 | pubmed:meshHeading | pubmed-meshheading:16352847... | lld:pubmed |
| pubmed-article:16352847 | pubmed:meshHeading | pubmed-meshheading:16352847... | lld:pubmed |
| pubmed-article:16352847 | pubmed:meshHeading | pubmed-meshheading:16352847... | lld:pubmed |
| pubmed-article:16352847 | pubmed:meshHeading | pubmed-meshheading:16352847... | lld:pubmed |
| pubmed-article:16352847 | pubmed:meshHeading | pubmed-meshheading:16352847... | lld:pubmed |
| pubmed-article:16352847 | pubmed:meshHeading | pubmed-meshheading:16352847... | lld:pubmed |
| pubmed-article:16352847 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16352847 | pubmed:articleTitle | Autoinducer 2 controls biofilm formation in Escherichia coli through a novel motility quorum-sensing regulator (MqsR, B3022). | lld:pubmed |
| pubmed-article:16352847 | pubmed:affiliation | Dept. of Chemical Engineering, University of Connecticut, 191 Auditorium Road, Storrs, CT 06269-3222, USA. | lld:pubmed |
| pubmed-article:16352847 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16352847 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
| pubmed-article:16352847 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
