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Bacteria use exogenous peptidoglycan as a danger signal to trigger biofilm formation
Max Planck Institute for Terrestrial Microbiology, Marburg, Germany; Antimicrobial Discovery Center, Department of Biology, Northeastern University, MA, Boston, Thailand.
Biozentrum, University of Basel, Basel, Switzerland.
Biozentrum, University of Basel, Basel, Switzerland.
Umeå universitet, Medicinska fakulteten, Molekylär Infektionsmedicin, Sverige (MIMS). Umeå universitet, Medicinska fakulteten, Umeå Centre for Microbial Research (UCMR). Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten).ORCID-id: 0000-0002-0450-1430
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2025 (engelsk)Inngår i: Nature Microbiology, E-ISSN 2058-5276, Vol. 10, nr 1, s. 144-157Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

For any organism, survival is enhanced by the ability to sense and respond to threats in advance. For bacteria, danger sensing among kin cells has been observed, but the presence or impacts of general danger signals are poorly understood. Here we show that different bacterial species use exogenous peptidoglycan fragments, which are released by nearby kin or non-kin cell lysis, as a general danger signal. Using microscopy and gene expression profiling of Vibrio cholerae, we find that even brief signal exposure results in a regulatory response that causes three-dimensional biofilm formation, which protects cells from a broad range of stresses, including bacteriophage predation. A diverse set of species (Pseudomonas aeruginosa, Acinetobacter baumannii, Staphylococcus aureus, Enterococcus faecalis) also respond to exogenous peptidoglycan by forming biofilms. As peptidoglycan from different Gram-negative and Gram-positive species triggered three-dimensional biofilm formation, we propose that this danger signal and danger response are conserved among bacteria.

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Springer Nature, 2025. Vol. 10, nr 1, s. 144-157
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URN: urn:nbn:se:umu:diva-234005DOI: 10.1038/s41564-024-01886-5ISI: 001388924600001PubMedID: 39753671Scopus ID: 2-s2.0-85213967811OAI: oai:DiVA.org:umu-234005DiVA, id: diva2:1927386
Forskningsfinansiär
EU, Horizon 2020, 716734Swedish Research CouncilKnut and Alice Wallenberg FoundationSwedish Cancer SocietyThe Kempe FoundationsTilgjengelig fra: 2025-01-14 Laget: 2025-01-14 Sist oppdatert: 2025-01-14bibliografisk kontrollert

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