• Author: Christner, Martin

    Institute for Medical Microbiology, Virology and Hygiene, University Medical Centre Hamburg‐Eppendorf, Germany

  • Author: Heinze, Constanze

    Institute for Medical Microbiology, Virology and Hygiene, University Medical Centre Hamburg‐Eppendorf, Germany

  • Author: Busch, Michael

    Institute for Medical Microbiology, Virology and Hygiene, University Medical Centre Hamburg‐Eppendorf, Germany

  • Author: Franke, Gefion

    Institute for Medical Microbiology, Virology and Hygiene, University Medical Centre Hamburg‐Eppendorf, Germany

  • Author: Hentschke, Moritz

    Institute for Medical Microbiology, Virology and Hygiene, University Medical Centre Hamburg‐Eppendorf, Germany

  • Author: Dühring, Sara Bayard

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

  • Author: Büttner, Henning

    Institute for Medical Microbiology, Virology and Hygiene, University Medical Centre Hamburg‐Eppendorf, Germany

  • Author: Kotasinska, Marta

    Institute for Medical Microbiology, Virology and Hygiene, University Medical Centre Hamburg‐Eppendorf, Germany

  • Author: Wischnewski, Victoria

    Institute for Medical Microbiology, Virology and Hygiene, University Medical Centre Hamburg‐Eppendorf, Germany

  • Author: Kroll, Gesche

    Institute for Medical Microbiology, Virology and Hygiene, University Medical Centre Hamburg‐Eppendorf, Germany

  • Author: Buck, Friedrich

    Institute for Clinical Chemistry University Medical Centre 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

    Institute for Medical Microbiology, Virology and Hygiene, University Medical Centre 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: 3
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