The Transcriptional Antiterminator RfaH Represses Biofilm Formation in Escherichia coli

Autor: Jörg Hacker, Kai Michaelis, Karin Lindner, Paolo Landini, Christophe Beloin, Ulrich Dobrindt, Jean-Marc Ghigo
Přispěvatelé: Génétique des Biofilms, Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS), Bayerische Julius-Maximilians University, Swiss Federal Insitute of Aquatic Science and Technology [Dübendorf] (EAWAG), Fonds der Chemischen Industrie, Bayerische Forschungsstiftung, Fondation BNP Parisbas grants, We thank Jean-Claude Lazzaroni for help in constructing the LPS mutant in E. coli K-12 strains, Peter Owen for the gift of an Ag43 antiserum, and Shaynoor Dramsi for help with immunodetection experiments. We also thank Alexander J. B. Zehnder, Jennifer Leeds, Philippe Delepelaire, and Gábor Nagy for helpful discussions and critical reading of the manuscript. We thank Barbara Plaschke, Birgit Schellberg, and Teresa Colangelo for excellent technical assistance and Claude Lebos and Brigitte Arbeille (Laboratoire de Biologie Cellulaire et Microscopie Electronique, Tours, France) for preparation of the SEM micrographs., Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS)
Jazyk: angličtina
Rok vydání: 2006
Předmět:
Lipopolysaccharides
[SDV]Life Sciences [q-bio]
Mutant
MESH: Adhesins
Escherichia coli

MESH: Virulence
medicine.disease_cause
MESH: Down-Regulation
Bacterial Adhesion
MESH: Adhesins
Bacterial/metabolism

0303 health sciences
MESH: Escherichia coli/pathogenicity
MESH: Gene Expression Regulation
Bacterial

Adhesins
Escherichia coli

Strain (chemistry)
biology
Virulence
Escherichia coli Proteins
MESH: Lipopolysaccharides/metabolism
Enterobacteriaceae
Phenotype
MESH: Peptide Elongation Factors/physiology
MESH: Escherichia coli/physiology
MESH: Escherichia coli Proteins/physiology
MESH: Peptide Elongation Factors/genetics
Bacterial Outer Membrane Proteins
MESH: Antigens
Bacterial/metabolism

MESH: Biofilms/growth & development
Down-Regulation
MESH: Escherichia coli/genetics
Genetics and Molecular Biology
Microbiology
MESH: Escherichia coli Proteins/metabolism
MESH: Trans-Activators/physiology
03 medical and health sciences
MESH: Escherichia coli Proteins/genetics
medicine
Bacteriology
Escherichia coli
MESH: Bacterial Adhesion
Adhesins
Bacterial

Molecular Biology
030304 developmental biology
Antigens
Bacterial

MESH: Trans-Activators/genetics
MESH: Bacterial Outer Membrane Proteins/metabolism
030306 microbiology
Biofilm
Gene Expression Regulation
Bacterial

biology.organism_classification
Peptide Elongation Factors
[SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology
Biofilms
Trans-Activators
rpoS
Zdroj: Journal of Bacteriology
Journal of Bacteriology, American Society for Microbiology, 2006, 188 (4), pp.1316-1331. ⟨10.1128/JB.188.4.1316-1331.2006⟩
Journal of Bacteriology, 2006, 188 (4), pp.1316-1331. ⟨10.1128/JB.188.4.1316-1331.2006⟩
ISSN: 0021-9193
1098-5530
DOI: 10.1128/JB.188.4.1316-1331.2006⟩
Popis: We investigated the influence of regulatory and pathogenicity island-associated factors (Hha, RpoS, LuxS, EvgA, RfaH, and tRNA 5 Leu ) on biofilm formation by uropathogenic Escherichia coli (UPEC) strain 536. Only inactivation of rfaH , which encodes a transcriptional antiterminator, resulted in increased initial adhesion and biofilm formation by E. coli 536. rfaH inactivation in nonpathogenic E. coli K-12 isolate MG1655 resulted in the same phenotype. Transcriptome analysis of wild-type strain 536 and an rfaH mutant of this strain revealed that deletion of rfaH correlated with increased expression of flu orthologs. flu encodes antigen 43 (Ag43), which mediates autoaggregation and biofilm formation. We confirmed that deletion of rfaH leads to increased levels of flu and flu -like transcripts in E. coli K-12 and UPEC. Supporting the hypothesis that RfaH represses biofilm formation through reduction of the Ag43 level, the increased-biofilm phenotype of E. coli MG1655 rfaH was reversed upon inactivation of flu . Deletion of the two flu orthologs, however, did not modify the behavior of mutant 536 rfaH . Our results demonstrate that the strong initial adhesion and biofilm formation capacities of strain MG1655 rfaH are mediated by both increased steady-state production of Ag43 and likely increased Ag43 presentation due to null rfaH -dependent lipopolysaccharide depletion. Although the roles of rfaH in the biofilm phenotype are different in UPEC strain 536 and K-12 strain MG1655, this study shows that RfaH, in addition to affecting the expression of bacterial virulence factors, also negatively controls expression and surface presentation of Ag43 and possibly another Ag43-independent factor(s) that mediates cell-cell interactions and biofilm formation.
Databáze: OpenAIRE