title: Glucose-related dissociation between icaADBC transcription and biofilm expression by Staphylococcus epidermidis: evidence for an additional factor required for polysaccharide intercellular adhesin synthesis.
abstract: Biofilm formation in Staphylococcus epidermidis depends, in the majority of the strains, on the activity of the icaADBC locus. The expression of the operon that encodes the synthetic enzymes of the intercellular polysaccharide adhesin (PIA) depends on a variety of exogenic environmental conditions and is, at least in part, regulated by the alternative sigma factor sigma(B). We investigated the transcriptional regulation of the ica operon and the respective phenotypes expressed under growth conditions differing in the content of glucose in the growth medium. In the presence of glucose, S. epidermidis exhibited a PIA- and biofilm-positive phenotype whereas ica transcription was down-regulated in the postexponential and stationary phases of growth. Surprisingly, maximum transcription of ica was detectable in the stationary phase of growth in the absence of glucose despite the expression of a PIA- and biofilm-negative phenotype. In vitro enzymatic assays and phenotypic characterization showed that the abundant amount of ica mRNA was functionally active because induction of stationary-phase cells with glucose led to immediate PIA synthesis. Induction of biofilm formation could be completely inhibited by chloramphenicol, which, given at a later stage of biofilm accumulation, also inhibited further development of preformed biofilm, indicating that continuous translation of an additional, icaADBC-independent factor is required for the expression of a biofilm-positive phenotype.
authors.affiliation: Institut für Medizinische Mikrobiologie und Immunologie, Universitätsklinikum Hamburg-Eppendorf, D-20246 Hamburg, Germany. dobinsky@uke.uni-hamburg.de
authors.forename: Sabine
authors.initials: S
authors.lastname: Dobinsky
authors.forename: Kathrin
authors.initials: K
authors.lastname: Kiel
authors.forename: Holger
authors.initials: H
authors.lastname: Rohde
authors.forename: Katrin
authors.initials: K
authors.lastname: Bartscht
authors.forename: Johannes K-M
authors.initials: JK
authors.lastname: Knobloch
authors.forename: Matthias A
authors.initials: MA
authors.lastname: Horstkotte
authors.forename: Dietrich
authors.initials: D
authors.lastname: Mack
mesh_terms: D018829:Adhesins, Bacterial / Q000096:biosynthesis*; D018441:Biofilms / Q000187:drug effects / Q000254:growth & development*; D015152:Blotting, Northern; D002701:Chloramphenicol / Q000494:pharmacology; D015964:Gene Expression Regulation, Bacterial; D005947:Glucose / Q000494:pharmacology / Q000502:physiology*; D017351:N-Acetylglucosaminyltransferases / Q000235:genetics* / Q000378:metabolism; D009876:Operon; D011135:Polysaccharides, Bacterial / Q000096:biosynthesis*; D011500:Protein Synthesis Inhibitors / Q000494:pharmacology; D012329:RNA, Bacterial / Q000235:genetics; D012333:RNA, Messenger / Q000032:analysis; D013212:Staphylococcus epidermidis / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D013997:Time Factors; D014158:Transcription, Genetic / Q000187:drug effects
chemical_list: D018829:Adhesins, Bacterial; D011135:Polysaccharides, Bacterial; D011500:Protein Synthesis Inhibitors; D012329:RNA, Bacterial; D012333:RNA, Messenger; C113579:polysaccharide intercellular adhesin; D002701:Chloramphenicol; D017351:N-Acetylglucosaminyltransferases; C037649:N-acetyllactosaminide beta-1,6-N-acetylglucosaminyltransferase; D005947:Glucose