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Breakdown of Vibrio cholerae biofilm architecture induced by antibiotics disrupts community barrier function.

ABSTRACT: Bacterial cells in nature are frequently exposed to changes in their chemical environment1,2. The response mechanisms of isolated cells to such stimuli have been investigated in great detail. By contrast, little is known about the emergent multicellular responses to environmental changes, such as antibiotic exposure3-7, which may hold the key to understanding the structure and functions of the most common type of bacterial communities: biofilms. Here, by monitoring all individual cells in Vibrio cholerae biofilms during exposure to antibiotics that are commonly administered for cholera infections, we found that translational inhibitors cause strong effects on cell size and shape, as well as biofilm architectural properties. We identified that single-cell-level responses result from the metabolic consequences of inhibition of protein synthesis and that the community-level responses result from an interplay of matrix composition, matrix dissociation and mechanical interactions between cells. We further observed that the antibiotic-induced changes in biofilm architecture have substantial effects on biofilm population dynamics and community assembly by enabling invasion of biofilms by bacteriophages and intruder cells of different species. These mechanistic causes and ecological consequences of biofilm exposure to antibiotics are an important step towards understanding collective bacterial responses to environmental changes, with implications for the effects of antimicrobial therapy on the ecological succession of biofilm communities.

SUBMITTER: Diaz-Pascual F

PROVIDER: S-EPMC6881181 | biostudies-literature | 2019 Dec

REPOSITORIES: biostudies-literature

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Breakdown of Vibrio cholerae biofilm architecture induced by antibiotics disrupts community barrier function.

Díaz-Pascual Francisco F Hartmann Raimo R Lempp Martin M Vidakovic Lucia L Song Boya B Jeckel Hannah H Thormann Kai M KM Yildiz Fitnat H FH Dunkel Jörn J Link Hannes H Nadell Carey D CD Drescher Knut K

Nature microbiology 20191028 12

Bacterial cells in nature are frequently exposed to changes in their chemical environment<sup>1,2</sup>. The response mechanisms of isolated cells to such stimuli have been investigated in great detail. By contrast, little is known about the emergent multicellular responses to environmental changes, such as antibiotic exposure<sup>3-7</sup>, which may hold the key to understanding the structure and functions of the most common type of bacterial communities: biofilms. Here, by monitoring all indi ...[more]

PMID: 31659297

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Project description:Vibrio cholerae biofilm biogenesis, which is important for survival, dissemination, and persistence, requires multiple genes in the Vibrio polysaccharides (vps) operons I and II as well as the cluster of ribomatrix (rbm) genes. Transcriptional control of these genes is a complex process that requires several activators/repressors and the ubiquitous signaling molecule, cyclic di-GMP (c-di-GMP). Previously, we demonstrated that VpsR directly activates RNA polymerase containing σ70 (σ70-RNAP) at the vpsL promoter (P vpsL ), which precedes the vps-II operon, in a c-di-GMP-dependent manner by stimulating formation of the transcriptionally active, open complex. Using in vitro transcription, electrophoretic mobility shift assays, and DNase I footprinting, we show here that VpsR also directly activates σ70-RNAP transcription from other promoters within the biofilm formation cluster, including P vpsU , at the beginning of the vps-I operon, P rbmA , at the start of the rbm cluster, and P rbmF , which lies upstream of the divergent rbmF and rbmE genes. In this capacity, we find that VpsR is able to behave both as a class II activator, which functions immediately adjacent/overlapping the core promoter sequence (P vpsL and P vpsU ), and as a class I activator, which functions farther upstream (P rbmA and P rbmF ). Because these promoters vary in VpsR-DNA binding affinity in the absence and presence of c-di-GMP, we speculate that VpsR's mechanism of activation is dependent on both the concentration of VpsR and the level of c-di-GMP to increase transcription, resulting in finely tuned regulation.IMPORTANCEVibrio cholerae, the bacterial pathogen that is responsible for the disease cholera, uses biofilms to aid in survival, dissemination, and persistence. VpsR, which directly senses the second messenger c-di-GMP, is a major regulator of this process. Together with c-di-GMP, VpsR directly activates transcription by RNA polymerase containing σ70 from the vpsL biofilm biogenesis promoter. Using biochemical methods, we demonstrate for the first time that VpsR/c-di-GMP directly activates σ70-RNA polymerase at the first genes of the vps and ribomatrix operons. In this regard, it functions as either a class I or class II activator. Our results broaden the mechanism of c-di-GMP-dependent transcription activation and the specific role of VpsR in biofilm formation.

Dataset Information

Breakdown of Vibrio cholerae biofilm architecture induced by antibiotics disrupts community barrier function.

Publications

Breakdown of Vibrio cholerae biofilm architecture induced by antibiotics disrupts community barrier function.

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