The TfoY regulon of Vibrio cholerae.
Ontology highlight
ABSTRACT:
ORGANISM(S): Vibrio cholerae
PROVIDER: GSE79467 | GEO | 2016/03/22
SECONDARY ACCESSION(S): PRJNA315898
REPOSITORIES: GEO
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Project description:In this study, we determined the TfoX regulon of V. cholerae WT strain A1552 compared to a ΔhapR and ΔqstR strain using RNA-seq to better understand the protein's function.
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Project description:In this study, we determined the TfoY regulon of V. cholerae using RNA-seq to better uderstand the protein's function. mRNA profiles of a WT V. cholerae O1 El Tor strain (A1552) and of a TfoY-producing derivative of the WT strain (A1552-TntfoY). 3 independent biological replicates are provided for each bacterial strain. The bacteria were grown to high cell density and in the presence of arabinose (to induce TfoY in strain A1552-TntfoY).
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Project description:In this study, we compared the QstR regulon to the TfoX regulon (and TfoY regulon) of V. cholerae in WT strain A1552 and its ΔhapRΔvpsA derivative using RNA-seq to better understand QstR's function.
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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
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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
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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
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
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
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 | GSE72471 | GEO
Project description:Using a combination of ChIP-seq and RNA-seq we show that ToxT regulates expression of the small RNA TarB. TarB modulates the expression level of the transcriptioanl repressor VC0177. VC0177 controls expression of several genes including VC0179. The function of the Vibrio 7th pandemic island-1 (VSP-1) in cholera pathogenesis has remained obscure. Utilizing ChIP-seq and RNA-seq to map the regulon of the master virulence regulator ToxT, we identify a TCP island encoded small RNA that reduces the expression of a previously unrecognized VSP-1 encoded transcription factor termed VspR. VspR modulates the expression of several VSP-1 genes including one that encodes a novel class of di-nucleotide cyclase (DncV), which preferentially synthesizes a previously undescribed hybrid cyclic AMP-GMP molecule. We show that DncV is required for efficient intestinal colonization and down-regulates V. cholerae chemotaxis, a phenotype previously associated with hyperinfectivity. This pathway couples the actions of previously disparate genomic islands, defines VSP-1 as a pathogenicity island in V. cholerae and implicates its occurrence in 7th pandemic strains as a benefit for host adaptation through the production of a regulatory cyclic di-nucleotide.
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