Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Identification of a bile acid-binding transcription factor in Clostridioides difficile using chemical proteomics

ABSTRACT: Identification of a bile acid-binding transcription factor in Clostridioides difficile using chemical proteomics

PROVIDER: PRJNA844117 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR19476104.fastq.gz	Fastqsanger.gz
	SRR19476105.fastq.gz	Fastqsanger.gz
	SRR19476106.fastq.gz	Fastqsanger.gz
	SRR19476107.fastq.gz	Fastqsanger.gz
	SRR19476108.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Identification of a bile acid-binding transcription factor in Clostridioides difficile using chemical proteomics

Project description:Clostridioides difficile is a Gram-positive anaerobic bacterium that is the leading cause of hospital-acquired gastroenteritis in the US. In the gut milieu, C. difficile encounters microbiota-derived bile acids capable of inhibiting its growth, which are thought to be a mechanism of colonization resistance. While the levels of certain bile acids in the gut correlate with susceptibility to C. difficile infection, their molecular targets in C. difficile remain unknown. In this study, we sought to use chemical proteomics to identify bile acid-interacting proteins in C. difficile. Using photoaffinity bile acid probes and chemical proteomics, we identified a previously uncharacterized MerR family protein, CD3583 (now BapR), as a putative bile acid-sensing transcription regulator. Our data indicate that BapR binds and is stabilized by lithocholic acid (LCA) in C. difficile. Although loss of BapR did not affect C. difficile's sensitivity to LCA, bapR mutant cells elongated more in the presence of LCA than wild-type cells. Transcriptomics revealed that BapR regulates the expression of the gene clusters mdeA-cd3573 and cd0618-cd0616, and cwpV, with the expression of the mdeA-cd3573 locus being specifically de-repressed in the presence of LCA in a BapR-dependent manner. Electrophoretic mobility shift assays revealed that BapR directly binds to the mdeA promoter region. Since mdeA is involved in amino acid-related sulfur metabolism and the mdeA-cd3573 locus encodes putative transporters, we propose that BapR senses a gastrointestinal tract-specific small molecule, LCA, as an environmental cue for metabolic adaptation.

2022-06-03 | GSE205226 | GEO

Clostridioides difficile: R20291_pMTL84151 transconjugant (C) vs. R20291_pMTL84151-03890 (T1)

Project description:Gene expression level of Clostridioides difficile (C. difficile) strain R20291 comparing control C. difficile carring pMTL84151 as vector plasmid with C. difficile conjugated with a pMTL84151-03890 gene. Goal was to determine the effects of 03890 gene conjugation on C. difficile strain R20291 gene expression.

2023-11-30 | GSE219066 | GEO

Clostridioides difficile responses to calprotectin

Project description:The intestines house a diverse microbiota that must compete for nutrients to survive, but the specific limiting nutrients that control pathogen colonization are not clearly defined. Clostridioides difficile colonization typically requires prior disruption of the microbiota, suggesting that outcompeting commensals for resources is key in establishing C. difficile infection (CDI). The immune protein calprotectin (CP) is released into the gut lumen during CDI to chelate zinc (Zn) and other essential nutrient metals. Yet, the impact of Zn limitation on C. difficile colonization is unknown. To define C. difficile responses to Zn limitation, we performed RNA sequencing on C. difficile exposed to CP. In media with CP, C. difficile upregulated genes involved in metal homeostasis and amino acid metabolism.

2019-10-24 | GSE135912 | GEO

Enterococci enhance Clostridioides difficile pathogenesis

Project description:Clostridioides difficile is one of the most common nosocomial pathogens and a global public health threat. Upon colonization of the gastrointestinal tract, C. difficile is exposed to a rapidly changing polymicrobial environment and a dynamic metabolic milieu. Despite the link between the gut microbiota and susceptibility to C. difficile, the impact of synergistic interactions between the microbiota and pathogens on the outcome of infection is largely unknown. Here, we show that microbial cooperation between C. difficile and Enterococcus has a profound impact on the growth, metabolism, and pathogenesis of C. difficile.. Through a process of nutrient restriction and metabolite cross-feeding, E. faecalis shapes the metabolic environment in the gut to enhance C. difficile fitness and increase toxin production. These findings demonstrate that members of the microbiota, such as Enterococcus, have a previously unappreciated impact on C. difficile behavior and virulence.

2022-09-17 | GSE165751 | GEO

Global transcriptome analysis of colonic tissue during Clostridioides difficile infection

Project description:Clostridioides difficile can cause severe infections in the gastrointestinal tract and affects almost half a million people in the U.S every year. Upon establishment of infection, a strong immune response is induced. We sought to investigate the dynamics of the mucosal host response during C. difficile infection.

2023-09-13 | GSE237574 | GEO

Dual RNA-seq identifies proteins and pathways required for Clostridioides difficile colonisation

Project description:Clostridioides difficile interactions with the gut mucosa are crucial for colonisation and establishment of infection, however key infection events during the establishment of disease are still poorly defined. To better understand the initial events that occur during C. difficile colonisation, we employed a dual RNA-sequencing approach to study the host and bacterial transcriptomic profiles during C. difficile infection in a dual-environment in vitro human gut model. Temporal changes in gene expression were analysed over 3-24h post infection and comparisons were made with uninfected controls.

2023-03-23 | E-MTAB-12660 | biostudies-arrayexpress

Clostridioides difficile toxins deregulate tight junction proteins.

Project description:The Clostridioides difficile toxins TcdA and TcdB are responsible for diarrhea and colitis. The aim of this project was to explore the effects of the toxins on epithelial barrier function and the molecular mechanisms for diarrhea and inflammation. RNA-seq of toxin-treated intestinal cell monolayers was performed to describe the C. difficile-mediated effects. mRNA profiles from intestinale epithelial cells were generated by deep sequencing using Illumina NovaSeq 6000. This data provide the basis for subsequent upstream regulator analysis.

2023-11-29 | GSE232704 | GEO

c-di-AMP signaling is required for bile salts resistance and long-term colonization by Clostridioides difficile

Project description:In this study, we showed for the first time that c-di-AMP is produced by C. difficile and controls the uptake of potassium, making it essential for growth. We found that c-di-AMP is involved in biofilm formation, cell wall homeostasis, osmotolerance as well as detergent and bile salt resistance in C. difficile. We identified BusR as a new regulator that binds c-di-AMP and represses the expression of the compatible solute transporter BusAA-AB. Interestingly, a busR mutant is highly resistant to a hyperosmotic or bile salt stress compared to the parental strain while a busAA mutant is more susceptible. A short exposure of C. difficile cells to bile salts resulted in a decrease of the c-di-AMP concentrations reinforcing the hypothesis that changes in membrane characteristics due to variations of the cellular turgor or membrane damages constitute a signal for the adjustment of the intracellular c-di-AMP concentration. In a colonization mouse model, a strain producing elevated c-di-AMP concentrations failed to persist in the gut in contrast to the parental strain. Thus, c-di-AMP is a signaling molecule with pleiotropic effects that controls osmolyte uptake to confer osmotolerance and bile salt resistance in C. difficile and that is important for colonization of the host.

2021-12-27 | GSE192529 | GEO

Differential view on the bile acids stress response of Clostridioides difficile

Project description:In this study, we aimed at the characterization of C. difficile’s stress response to the main four human bile acids. Although, a phenotypically description of growth differences upon challenge with different bile acids has been described (Lewis 2016, Thanissery 2017), there is no information on the adaptation of gene expression available. We employed a comprehensive proteomics approach to record stress signatures of the unconjugated bile acids CA, CDCA, DCA and LCA in shock experiments as well as during long-term-stress conditions and could depict a general stress response concerning all four bile acids, but also specific responses to only a single or a few of the different bile acids. Our results are a starting point for the understanding of how the individual bile acids cocktail of a patient can decide on the outcome of a C. difficile infection.

2019-02-12 | PXD010514 | Pride

Chemical characterization of clostridithiol compounds in Clostridioides difficile

Project description:Stable isotope labeling of clostridithiol compounds 1-8 in liquid cultures of Clostridioides difficile upon supplementation of polyamines & relevant precursors containing carbon-13/deuterium labels in a modified minimal media. MS/MS of targeted compounds was collected at 30 eV collision energy. Datafiles for purified synthetic standards are also provided for comparison.

2025-06-12 | MSV000098168 | MassIVE

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data