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The cell wall lipoprotein CD1687 acts as a DNA binding protein during deoxycholate-induced biofilm formation in Clostridioides difficile

ABSTRACT: The cell wall lipoprotein CD1687 acts as a DNA binding protein during deoxycholate-induced biofilm formation in Clostridioides difficile

PROVIDER: PRJNA903906 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22361200.fastq.gz	Fastqsanger.gz
	SRR22361185.fastq.gz	Fastqsanger.gz
	SRR22361186.fastq.gz	Fastqsanger.gz
	SRR22361187.fastq.gz	Fastqsanger.gz
	SRR22361188.fastq.gz	Fastqsanger.gz

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Similar Datasets

The cell wall lipoprotein CD1687 acts as a DNA binding protein during deoxycholate-induced biofilm formation in Clostridioides difficile

Project description:The ability of bacterial pathogens to establish recurrent and persistent infections is frequently associated with their ability to form biofilms. Clostridioides difficile infections have a high rate of recurrence and relapses and it is hypothesised that biofilms are involved in its pathogenicity and persistence. Biofilm formation by C. difficile is still poorly understood. It has been shown that specific molecules such as deoxycholate (DCA) or metronidazole induce biofilm formation, but the mechanisms involved remain elusive. In this study, we describe the role of the lipoprotein CD1687 in the DCA-induced biofilm formation of C. difficile. We showed that the expression of CD1687, which is part of an operon within the CD1685-CD1689 gene cluster, is controlled by multiple transcription starting sites induced for some of them in response to DCA. Only CD1687 is required for biofilm formation and the overexpression of CD1687 is sufficient to induce biofilm formation. Using RNAseq analysis, we showed that CD1687 affects the expression of transporters and metabolic pathways and we identified several potential binding partners by pull-down assay, including transport-associated extracellular proteins. We then demonstrated that CD1687 is surface exposed in C. difficile, and this localization is required for DCA-induced biofilm formation. Given this localization and that C. difficile forms eDNA-rich biofilms, we confirmed that CD1687 binds DNA in a non-specific manner. We thus hypothesize that CD1687 is a component of the downstream response to DCA leading to biofilm formation by promoting interaction between the cells and the biofilm matrix by binding eDNA.

2023-04-19 | GSE218475 | GEO

The cell wall lipoprotein CD1687 acts as a DNA binding protein during deoxycholate-induced biofilm formation in Clostridioides difficile

2023-05-16 | PXD038282 | Pride

The cell wall lipoprotein CD1687 acts as a DNA binding protein during deoxycholate-induced biofilm formation in Clostridioides difficile.

Project description:The ability of bacterial pathogens to establish recurrent and persistent infections is frequently associated with their ability to form biofilms. Clostridioides difficile infections have a high rate of recurrence and relapses and it is hypothesized that biofilms are involved in its pathogenicity and persistence. Biofilm formation by C. difficile is still poorly understood. It has been shown that specific molecules such as deoxycholate (DCA) or metronidazole induce biofilm formation, but the mechanisms involved remain elusive. In this study, we describe the role of the C. difficile lipoprotein CD1687 during DCA-induced biofilm formation. We showed that the expression of CD1687, which is part of an operon within the CD1685-CD1689 gene cluster, is controlled by multiple transcription starting sites and some are induced in response to DCA. Only CD1687 is required for biofilm formation and the overexpression of CD1687 is sufficient to induce biofilm formation. Using RNAseq analysis, we showed that CD1687 affects the expression of transporters and metabolic pathways and we identified several potential binding partners by pull-down assay, including transport-associated extracellular proteins. We then demonstrated that CD1687 is surface exposed in C. difficile, and that this localization is required for DCA-induced biofilm formation. Given this localization and the fact that C. difficile forms eDNA-rich biofilms, we confirmed that CD1687 binds DNA in a non-specific manner. We thus hypothesize that CD1687 is a component of the downstream response to DCA leading to biofilm formation by promoting interaction between the cells and the biofilm matrix by binding eDNA.

| S-EPMC10175255 | biostudies-literature

Expression profile for BW25113 ΔmqsRA with deoxycholate stress

Project description:MqsR/MqsA is a well-characterized toxin/antitoxin system with several regulatory roles. Deletion of mqsRA reduced growth with deoxycholate stress. Here we performed a microarray to determine the expression profile with and without mqsRA under deoxycholate stress to determine transcriptional regulation.

2015-01-09 | GSE59441 | GEO

Deoxycholate induces biofilm formation by Clostridium difficile while repressing sporuation and toxin production

Project description:The objective of our study was to characterize the response of C. difficle to deoxycholate. When C. difficile was grown in the presence of deoxycholate, we observed an increase in biofilm formation. We then analyzed the transcriptome of the DCA-induced biofilm and cells grown in the absence of deoxycholate. The transcriptome analysis was then confirmed using phenotypic assays and gene-deletion strains.

2019-04-05 | GSE103952 | GEO

Expression profile for BW25113 M-NM-^TmqsRA with deoxycholate stress

2015-01-09 | E-GEOD-59441 | biostudies-arrayexpress

The food-borne pathogen Campylobacter jejuni responds to the bile salt deoxycholate with countermeasures to reactive oxygen species

Project description:Bile plays an important role in digestion, absorption of fats, and the excretion of waste products, while concurrently providing a critical barrier against colonization by harmful bacteria. Previous studies have demonstrated that gut pathogens react to bile by adapting their protein synthesis. The ability of pathogens to respond to bile is remarkably complex and still incompletely understood. Here we show that Campylobacter jejuni, a leading bacterial cause of human diarrheal illness worldwide, responds to deoxycholate, a component of bile, by altering global gene transcription in a manner consistent with a strategy to mitigate exposure to reactive oxygen stress. More specifically, continuous growth of C. jejuni in deoxycholate was found to: 1) induce the production of reactive oxygen species (ROS); 2) decrease succinate dehydrogenase activity (complex II of the electron transport chain); 3) increase catalase activity that is involved in H2O2 breakdown; and 4) result in DNA strand breaks. Congruently, by adding 4-hydroxy-TEMPO (TEMPOL), a superoxide dismutase mimic, that reacts with superoxide to cultures under deoxycholate-mediated ROS stress, C. jejuni growth in the presence of deoxycholate was rescued. We postulate that continuous exposure of a number of enteric pathogens to deoxycholate stimulates a conserved survival response to this stressor.

2017-11-13 | GSE89641 | GEO

Clostridium difficile Biofilm with and without deoxycholate at 48H

Project description:To understand the molecular mechanisms induced by deoxycholate (DCA) during biofilm formation and to identify factors implicated in the strong density of biofilms in this condition, we performed a transcriptomic analysis using microarrays. The microarrays were used to compare C. difficile transcription profiles of a 48 h biofilm (in BHISG medium) treated with DCA with an untreated biofilm.

2021-08-01 | GSE85982 | GEO

RNA-seq of Clostridioides difficile ∆rpoN mutant against wild-type control

Project description:The experiment intends to reveal the difference in gene expression profiles between the wild-type strain and the ∆rpoN mutant of Clostridioides difficile. We first constructed the ∆rpoN mutant, and the phenotypic changes of the ∆rpoN mutant against the wild-type strain were studied. To further elucidate the mechanism of phenotypic changes of the ∆rpoN mutant, RNA-sequencing experiments were carried out to reveal the underlying mechanism of phenotypic changes.

2024-12-30 | E-MTAB-14512 | biostudies-arrayexpress

RNA-seq of Clostridioides difficile ∆cwp66 mutant against wild-type control

Project description:The experiment intends to reveal the difference in gene expression profiles between the wild-type strain and the ∆cwp66 mutant of Clostridioides difficile. We first constructed the ∆cwp66 mutant, and the phenotypic changes of the ∆cwp66 mutant against the wild-type strain were studied. To further elucidate the mechanism of phenotypic changes of the ∆cwp66 mutant, RNA-sequencing experiments were carried out to reveal the underlying mechanism of phenotypic changes.

2022-03-01 | E-MTAB-11180 | biostudies-arrayexpress

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