Source:http://linkedlifedata.com/resource/pubmed/id/17827157
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
46
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pubmed:dateCreated |
2007-11-12
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pubmed:abstractText |
The invasion of intestinal epithelial cells by the Crohn disease-associated adherent-invasive Escherichia coli (AIEC) strain LF82 depends on surface appendages, such as type 1 pili and flagella. The absence of flagella in the AIEC strain LF82 results in a concomitant loss of type 1 pili. Here, we show that flagellar regulators, transcriptional activator FlhD(2)C(2), and sigma factor FliA are involved in the coordination of flagellar and type 1 pili synthesis. In the deletion mutants lacking these regulators, type 1 pili synthesis, adhesion, and invasion were severely decreased. FliA expressed alone in trans was sufficient to restore these defects in both the LF82-DeltaflhD and LF82-DeltafliA mutants. We related the loss of type 1 pili to the decreased expression of the FliA-dependent yhjH gene in the LF82-DeltafliA mutant. YhjH is an EAL domain phosphodiesterase involved in degradation of the bacterial second messenger cyclic dimeric GMP (c-di-GMP). Increased expression of either yhjH or an alternative c-di-GMP phosphodiesterase, yahA, partially restored type 1 pili synthesis, adhesion, and invasion in the LF82-DeltafliA mutant. Deletion of the GGDEF domain diguanylate cyclase gene, yaiC, involved in c-di-GMP synthesis in the LF82-DeltafliA mutant also partially restored these defects, whereas overexpression of the c-di-GMP receptor YcgR had the opposite effect. These findings show that in the AIEC strain LF82, FliA is a key regulatory component linking flagellar and type 1 pili synthesis and that its effect on type 1 pili is mediated, at least in part, via a c-di-GMP-dependent pathway.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0021-9258
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
16
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pubmed:volume |
282
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
33275-83
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:17827157-Crohn Disease,
pubmed-meshheading:17827157-Cyclic GMP,
pubmed-meshheading:17827157-Dimerization,
pubmed-meshheading:17827157-Escherichia coli,
pubmed-meshheading:17827157-Fimbriae, Bacterial,
pubmed-meshheading:17827157-Gene Expression Regulation, Bacterial,
pubmed-meshheading:17827157-Intestines,
pubmed-meshheading:17827157-Microscopy, Electron, Transmission,
pubmed-meshheading:17827157-Models, Biological,
pubmed-meshheading:17827157-Mutation,
pubmed-meshheading:17827157-Protein Structure, Tertiary,
pubmed-meshheading:17827157-Sigma Factor,
pubmed-meshheading:17827157-Transcription, Genetic,
pubmed-meshheading:17827157-Transcription Factors,
pubmed-meshheading:17827157-Transcriptional Activation
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pubmed:year |
2007
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pubmed:articleTitle |
The flagellar sigma factor FliA regulates adhesion and invasion of Crohn disease-associated Escherichia coli via a cyclic dimeric GMP-dependent pathway.
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pubmed:affiliation |
Université Clermont 1, Pathogénie Bactérienne Intestinale, Institut National de la Recherche Agronomique, Unité Sous Contrat 2018 (USC INRA 2018), Clermont-Ferrand F-63001, France. laurent.claret@u-clermont1.fr
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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