• Author: Christner, Martin

    University Medical Center Hamburg-Eppendorf, Germany

  • Author: Heinze, Constanze

    University Medical Center Hamburg-Eppendorf, Germany

  • Author: Busch, Michael

    University Medical Center Hamburg-Eppendorf, Germany

  • Author: Franke, Gefion

    University Medical Center Hamburg-Eppendorf, Germany

  • Author: Hentschke, Moritz

    University Medical Center Hamburg-Eppendorf, Germany

  • Author: Dühring, Sara Bayard

    Center for Systems Microbiology, Department of Systems Biology, Technical University of Denmark

  • Author: Büttner, Henning

    University Medical Center Hamburg-Eppendorf, Germany

  • Author: Kotasinska, Marta

    University Medical Center Hamburg-Eppendorf, Germany

  • Author: Wischnewski, Victoria

    University Medical Center Hamburg-Eppendorf, Germany

  • Author: Kroll, Gesche

    University Medical Center Hamburg-Eppendorf, Germany

  • Author: Buck, Friedrich

    University Medical Center Hamburg-Eppendorf

  • Author: Molin, Søren

    Center for Systems Microbiology, Department of Systems Biology, Technical University of Denmark, Matematiktorvet, DK-2800, Lyngby, Denmark

  • Author: Otto, Michael

    National Institutes of Health, United States

  • Author: Rohde, Holger

    University Medical Center Hamburg-Eppendorf, Germany

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Biofilm formation is essential for Staphylococcus epidermidis pathogenicity in implant‐associated infections. Nonetheless, large proportions of invasive Staphylococcus epidermidis isolates fail to form a biofilm in vitro. We here tested the hypothesis that this apparent paradox is related to the existence of superimposed regulatory systems suppressing a multicellular biofilm life style in vitro. Transposon mutagenesis of clinical significant but biofilm‐negative S. epidermidis 1585 was used to isolate a biofilm positive mutant carrying a Tn917 insertion in sarA, chief regulator of staphylococcal virulence. Genetic analysis revealed that inactivation of sarA induced biofilm formation via overexpression of the giant 1 MDa extracellular matrix binding protein (Embp), serving as an intercellular adhesin. In addition to Embp, increased extracellular DNA (eDNA) release significantly contributed to biofilm formation in mutant 1585ΔsarA. Increased eDNA amounts indirectly resulted from upregulation of metalloprotease SepA, leading to boosted processing of autolysin AtlE, in turn inducing augmented autolysis and release of eDNA. Hence, this study identifies sarA as a negative regulator of Embp‐ and eDNA‐dependent biofilm formation. Given the importance of SarA as a positive regulator of polysaccharide mediated cell aggregation, the regulator enables S. epidermidis to switch between mechanisms of biofilm formation, ensuring S. epidermidis adaptation to hostile environments.
Original languageEnglish
JournalMolecular Microbiology
Publication date2012
Volume86
Issue2
Pages394-410
ISSN0950-382X
DOIs
StatePublished
CitationsWeb of Science® Times Cited: 11
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