Identification of signaling pathways, matrix-digestion enzymes, and motility components controlling biofilm dispersal.

TitleIdentification of signaling pathways, matrix-digestion enzymes, and motility components controlling biofilm dispersal.
Publication TypeJournal Article
Year of Publication2020
AuthorsBridges, AA, Fei, C, Bassler, BL
JournalProc Natl Acad Sci U S A
Volume117
Issue51
Pagination32639-32647
Date Published2020 12 22
ISSN1091-6490
KeywordsAdhesins, Bacterial, Anti-Bacterial Agents, Bacterial Proteins, Biofilms, Cyclic GMP, Enzymes, Gene Expression Regulation, Bacterial, Mutation, Operon, Signal Transduction, Time-Lapse Imaging, Vibrio cholerae
Abstract

<p>Bacteria alternate between being free-swimming and existing as members of sessile multicellular communities called biofilms. The biofilm lifecycle occurs in three stages: cell attachment, biofilm maturation, and biofilm dispersal. biofilms are hyperinfectious, and biofilm formation and dispersal are considered central to disease transmission. While biofilm formation is well studied, almost nothing is known about biofilm dispersal. Here, we conducted an imaging screen for mutants that fail to disperse, revealing three classes of dispersal components: signal transduction proteins, matrix-degradation enzymes, and motility factors. Signaling proteins dominated the screen and among them, we focused on an uncharacterized two-component sensory system that we term DbfS/DbfR for dispersal of biofilm sensor/regulator. Phospho-DbfR represses biofilm dispersal. DbfS dephosphorylates and thereby inactivates DbfR, which permits dispersal. Matrix degradation requires two enzymes: LapG, which cleaves adhesins, and RbmB, which digests matrix polysaccharides. Reorientation in swimming direction, mediated by CheY3, is necessary for cells to escape from the porous biofilm matrix. We suggest that these components act sequentially: signaling launches dispersal by terminating matrix production and triggering matrix digestion, and subsequent cell motility permits escape from biofilms. This study lays the groundwork for interventions aimed at modulating biofilm dispersal to ameliorate disease.</p>

DOI10.1073/pnas.2021166117
Alternate JournalProc Natl Acad Sci U S A
PubMed ID33288715
PubMed Central IDPMC7768729
Grant ListR37 GM065859 / GM / NIGMS NIH HHS / United States
DRG-2302-17 / HHMI / Howard Hughes Medical Institute / United States