Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Characterization of the HNS Regulon Vibrio cholerae El Tor

ABSTRACT: The transcriptional factor ToxR initiates a virulence regulatory cascade required for V. cholerae to express critical host colonization factors and cause disease. Genome-wide expression studies suggest that ToxR regulates many genes important for V. cholerae pathogenesis, yet our knowledge of the direct regulon controlled by ToxR is limited to just four genes. Here, we determine ToxR’s genome-wide DNA-binding profile and show that ToxR is a global regulator of both progenitor genome-encoded genes and horizontally acquired islands encoding the majority of V. cholerae’s major virulence factors. Our results suggest that ToxR has gained regulatory control over important acquired elements that not only drive V. cholerae pathogenesis but that also define the major transitions of V. cholerae pandemic lineages. We demonstrate that ToxR shares nearly half its regulon with the histone-like nucleoid structuring protein H-NS, and antagonizes H-NS for control of critical colonization functions. This regulatory interaction is the major role of ToxR in V. cholerae colonization since deletion of H-NS abrogates the need of ToxR in V. cholerae host colonization. By comparing the genome-wide binding profiles of ToxR and other critical virulence regulators, we show that despite similar predicted DNA binding requirements, ToxR is unique in its global control of progenitor-encoded and acquired genes. Our results suggest that, like H-NS, factors in addition to linear DNA sequence drive selection of ToxR binding sites.

ORGANISM(S): Vibrio cholerae O1 str. C6706

PROVIDER: GSE72471 | GEO | 2016/03/23

SECONDARY ACCESSION(S): PRJNA294113

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Characterization of the ToxR Regulon Vibrio cholerae El Tor

Project description:The transcriptional factor ToxR initiates a virulence regulatory cascade required for V. cholerae to express critical host colonization factors and cause disease. Genome-wide expression studies suggest that ToxR regulates many genes important for V. cholerae pathogenesis, yet our knowledge of the direct regulon controlled by ToxR is limited to just four genes. Here, we determine ToxRâs genome-wide DNA-binding profile and show that ToxR is a global regulator of both progenitor genome-encoded genes and horizontally acquired islands encoding the majority of V. choleraeâs major virulence factors. Our results suggest that ToxR has gained regulatory control over important acquired elements that not only drive V. cholerae pathogenesis but that also define the major transitions of V. cholerae pandemic lineages. We demonstrate that ToxR shares nearly half its regulon with the histone-like nucleoid structuring protein H-NS, and antagonizes H-NS for control of critical colonization functions. This regulatory interaction is the major role of ToxR in V. cholerae colonization since deletion of H-NS abrogates the need of ToxR in V. cholerae host colonization. By comparing the genome-wide binding profiles of ToxR and other critical virulence regulators, we show that despite similar predicted DNA binding requirements, ToxR is unique in its global control of progenitor-encoded and acquired genes. Our results suggest that, like H-NS, factors in addition to linear DNA sequence drive selection of ToxR binding sites. We used ChIP-seq to identify ToxR binding sites across the genome to determine the direct regulon of ToxR

2016-03-23 | E-GEOD-72473 | biostudies-arrayexpress

Characterization of the HNS Regulon Vibrio cholerae El Tor

Project description:The transcriptional factor ToxR initiates a virulence regulatory cascade required for V. cholerae to express critical host colonization factors and cause disease. Genome-wide expression studies suggest that ToxR regulates many genes important for V. cholerae pathogenesis, yet our knowledge of the direct regulon controlled by ToxR is limited to just four genes. Here, we determine ToxRâs genome-wide DNA-binding profile and show that ToxR is a global regulator of both progenitor genome-encoded genes and horizontally acquired islands encoding the majority of V. choleraeâs major virulence factors. Our results suggest that ToxR has gained regulatory control over important acquired elements that not only drive V. cholerae pathogenesis but that also define the major transitions of V. cholerae pandemic lineages. We demonstrate that ToxR shares nearly half its regulon with the histone-like nucleoid structuring protein H-NS, and antagonizes H-NS for control of critical colonization functions. This regulatory interaction is the major role of ToxR in V. cholerae colonization since deletion of H-NS abrogates the need of ToxR in V. cholerae host colonization. By comparing the genome-wide binding profiles of ToxR and other critical virulence regulators, we show that despite similar predicted DNA binding requirements, ToxR is unique in its global control of progenitor-encoded and acquired genes. Our results suggest that, like H-NS, factors in addition to linear DNA sequence drive selection of ToxR binding sites. We used ChIP-seq to identify HNS binding sites across the genome to determine the direct regulon of HNS

2016-03-23 | E-GEOD-72471 | biostudies-arrayexpress

Characterization of the TcpP Regulon Vibrio cholerae El Tor

Project description:The transcriptional factor ToxR initiates a virulence regulatory cascade required for V. cholerae to express critical host colonization factors and cause disease. Genome-wide expression studies suggest that ToxR regulates many genes important for V. cholerae pathogenesis, yet our knowledge of the direct regulon controlled by ToxR is limited to just four genes. Here, we determine ToxRâ??s genome-wide DNA-binding profile and show that ToxR is a global regulator of both progenitor genome-encoded genes and horizontally acquired islands encoding the majority of V. choleraeâ??s major virulence factors. Our results suggest that ToxR has gained regulatory control over important acquired elements that not only drive V. cholerae pathogenesis but that also define the major transitions of V. cholerae pandemic lineages. We demonstrate that ToxR shares nearly half its regulon with the histone-like nucleoid structuring protein H-NS, and antagonizes H-NS for control of critical colonization functions. This regulatory interaction is the major role of ToxR in V. cholerae colonization since deletion of H-NS abrogates the need of ToxR in V. cholerae host colonization. By comparing the genome-wide binding profiles of ToxR and other critical virulence regulators, we show that despite similar predicted DNA binding requirements, ToxR is unique in its global control of progenitor-encoded and acquired genes. Our results suggest that, like H-NS, factors in addition to linear DNA sequence drive selection of ToxR binding sites. We used ChIP-seq to identify TcpP binding sites across the genome to determine the direct regulon of TcpP

2016-03-23 | E-GEOD-72472 | biostudies-arrayexpress

Characterization of the ToxR Regulon Vibrio cholerae El Tor

Project description:The transcriptional factor ToxR initiates a virulence regulatory cascade required for V. cholerae to express critical host colonization factors and cause disease. Genome-wide expression studies suggest that ToxR regulates many genes important for V. cholerae pathogenesis, yet our knowledge of the direct regulon controlled by ToxR is limited to just four genes. Here, we determine ToxR’s genome-wide DNA-binding profile and show that ToxR is a global regulator of both progenitor genome-encoded genes and horizontally acquired islands encoding the majority of V. cholerae’s major virulence factors. Our results suggest that ToxR has gained regulatory control over important acquired elements that not only drive V. cholerae pathogenesis but that also define the major transitions of V. cholerae pandemic lineages. We demonstrate that ToxR shares nearly half its regulon with the histone-like nucleoid structuring protein H-NS, and antagonizes H-NS for control of critical colonization functions. This regulatory interaction is the major role of ToxR in V. cholerae colonization since deletion of H-NS abrogates the need of ToxR in V. cholerae host colonization. By comparing the genome-wide binding profiles of ToxR and other critical virulence regulators, we show that despite similar predicted DNA binding requirements, ToxR is unique in its global control of progenitor-encoded and acquired genes. Our results suggest that, like H-NS, factors in addition to linear DNA sequence drive selection of ToxR binding sites.

2016-03-23 | GSE72473 | GEO

Characterization of the TcpP Regulon Vibrio cholerae El Tor

Project description:The transcriptional factor ToxR initiates a virulence regulatory cascade required for V. cholerae to express critical host colonization factors and cause disease. Genome-wide expression studies suggest that ToxR regulates many genes important for V. cholerae pathogenesis, yet our knowledge of the direct regulon controlled by ToxR is limited to just four genes. Here, we determine ToxR’s genome-wide DNA-binding profile and show that ToxR is a global regulator of both progenitor genome-encoded genes and horizontally acquired islands encoding the majority of V. cholerae’s major virulence factors. Our results suggest that ToxR has gained regulatory control over important acquired elements that not only drive V. cholerae pathogenesis but that also define the major transitions of V. cholerae pandemic lineages. We demonstrate that ToxR shares nearly half its regulon with the histone-like nucleoid structuring protein H-NS, and antagonizes H-NS for control of critical colonization functions. This regulatory interaction is the major role of ToxR in V. cholerae colonization since deletion of H-NS abrogates the need of ToxR in V. cholerae host colonization. By comparing the genome-wide binding profiles of ToxR and other critical virulence regulators, we show that despite similar predicted DNA binding requirements, ToxR is unique in its global control of progenitor-encoded and acquired genes. Our results suggest that, like H-NS, factors in addition to linear DNA sequence drive selection of ToxR binding sites.

2016-03-23 | GSE72472 | GEO

Gene expression analysis of Photobacterium profundum DB110 and TW30 toxR mutant strain at 0.1 MPa and 28 MPa

2012-12-22 | GSE38259 | GEO

Gene expression analysis of Photobacterium profundum DB110 and TW30 toxR mutant strain at 0.1 MPa and 28 MPa

Project description:Here we report the massively parallel cDNA sequencing (RNA-seq) analysis performed using high throughput sequencing of wild type (DB110) and toxR (TW30) mutant strains of the deep-sea bacterium Photobacterium profundum. ToxR is a transmembrane DNA-binding protein first discovered in Vibrio cholerae and able to regulate numerous genes involved in virulence. In P. profundum the abundance and activity of the same protein is influenced by hydrostatic pressure and is able to regulate genes in a pressure-dependent manner. To better characterize the ToxR regulon, we have compared the genes differentially expressed in response to pressure changes with those whose expression is altered between wild type and toxR mutant strains. Four samples were analyzed: DB110 strain grown at 0.1 MPa, DB110 strain grown at 28 MPa, TW30 strain grown at 0.1 MPa, TW30 strain grown at 28 MPa. Two independent coltures (replicates) were grown for each sample, RNA was extracted from each replicate and RNAs from the two replicates were pooled together to reduce biological variability. No replicates were included in experimental design.

2012-12-22 | E-GEOD-38259 | biostudies-arrayexpress

TsrA regulates gene expression of horizontally acquired elements in Vibrio cholerae via both H-NS dependent and independent mechanisms [RNA-Seq]

Project description:Vibrio cholerae, the causative agent of the diarrheal disease cholera, poses an ongoing health threat due to its wide repertoire of horizontally acquired elements (HAEs) and virulence factors. New clinical isolates of the bacterium with improved fitness abilities, often associated with HAEs, frequently emerge. The appropriate control and expression of such genetic elements is critical for the bacteria to thrive in different environments. H-NS, the histone-like nucleoid structuring protein, is the best studied xenogeneic silencer of HAEs in gamma-proteobacteria. Although H-NS and other highly abundant nucleoid-associated proteins (NAPs) have been shown to play important roles in regulating HAEs and virulence in model bacteria, we still lack a comprehensive understanding of how different NAPs modulate transcription in V. cholerae. By obtaining genome-wide measurements of protein occupancy and active transcription in a clinical isolate of V. cholerae, harboring recently-discovered HAEs encoding for phage defense systems, we show that lack of H-NS causes a robust increase on the expression of genes found in many HAEs. We further found that TsrA, a protein with partial homology to H-NS, regulates virulence genes primarily through modulation of H-NS activity, but we also found a few sites that are affected by TsrA independently of H-NS. Our results demonstrate how the combinatorial activity of NAPs is employed by a clinical isolate of an important pathogen to regulate recently-discovered HAEs.

2024-02-09 | GSE250406 | GEO

TsrA regulates gene expression of horizontally acquired elements in Vibrio cholerae via both H-NS dependent and independent mechanisms [IPOD-HR]

2024-02-09 | GSE250405 | GEO

Exploiting Dynamics of Genomic Islands to Edit the Genome of Vibrio cholerae and Identify Novel Interactions Between Core and Acquired Genome

Project description:Horizontally acquired genetic elements (HGEs) plays a major for determination of virulence, antimicrobial resistance, adaptation and evolution in pathogenic bacteria. Conserved integrative mobile genetic elements (MGEs) of Vibrio cholerae contribute in the disease development, antimicrobial resistance and metabolic functions. To understand the dynamics of integrative MGEs and cross talk between MGEs and core genome, engineered genome of V. cholerae was monitored in the presence and absence of horizontally acquired genetic elements. Deletion of more than 250 revealed that CTX contributes to the essentiality of SOS response master regulator LexA in V. cholerae. Also, he core genome encoded RecA helps CTX to bypass the host immunity and replicate in the host cell in the presence of similar prophage in the host chromosome. Finally, our multiomics data reveal importance of MGEs in modulating the level of cellular proteome and metabolome in V. cholerae. This study for the first time engineered the genome of V. cholerae strains to eliminate all the GIs, ICE and prophages from their genome and revealed new interactions between core and acquired genomes. The engineered strain could be a potential candidate for understanding evolution of cholera pathogen and development of therapeutics.

2020-09-28 | PXD017801 | Pride

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