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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Vibrio cholerae

PROVIDER: GSE250408 | GEO | 2024/02/09

REPOSITORIES: GEO

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

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 | GSE250405 | GEO

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

2024-02-09 | GSE250406 | GEO

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

Project description:TsrA regulates gene expression of horizontally acquired elements in Vibrio cholerae via both H-NS dependent and independent mechanisms

| PRJNA1053818 | ENA

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

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

| PRJNA1053821 | ENA

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

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

| PRJNA1053825 | ENA

ToxR Antagonizes H-NS Regulation of Horizontally Acquired Genes to Drive Host Colonization.

Project description:The virulence regulator ToxR initiates and coordinates gene expression needed by Vibrio cholerae to colonize the small intestine and cause disease. Despite its prominence in V. cholerae virulence, our understanding of the direct ToxR regulon is limited to four genes: toxT, ompT, ompU and ctxA. Here, we determine ToxR's genome-wide DNA-binding profile and demonstrate that ToxR is a global regulator of both progenitor genome-encoded genes and horizontally acquired islands that encode V. cholerae's major virulence factors and define pandemic lineages. We show that ToxR shares more than a third of its regulon with the histone-like nucleoid structuring protein H-NS, and antagonizes H-NS binding at shared binding locations. Importantly, we demonstrate that this regulatory interaction is the critical function of ToxR in V. cholerae colonization and biofilm formation. In the absence of H-NS, ToxR is no longer required for V. cholerae to colonize the infant mouse intestine or for robust biofilm formation. We further illustrate a dramatic difference in regulatory scope between ToxR and other prominent virulence regulators, despite similar predicted requirements for DNA binding. Our results suggest that factors in addition to primary DNA structure influence the ability of ToxR to recognize its target promoters.

| S-EPMC4829181 | biostudies-literature

H-NS binding and repression of the ctx promoter in Vibrio cholerae.

Project description:Expression of the ctx and tcp genes, which encode cholera toxin and the toxin coregulated pilus, the Vibrio cholerae O1 virulence determinants having the largest contribution to cholera disease, is repressed by the nucleoid-associated protein H-NS and activated by the AraC-like transcriptional regulator ToxT. To elucidate the molecular mechanism by which H-NS controls transcription of the ctxAB operon, H-NS repression and binding were characterized by using a promoter truncation series, gel mobility shift assays, and DNase I footprinting. Promoter regions found to be important for H-NS repression correlated with in vitro binding. Four main H-NS binding regions are present at ctx. One region overlaps the high-affinity ToxT binding site and extends upstream, another overlaps the ToxT low-affinity binding site around the -35 element, and the remaining two are located adjacent to one another downstream of the transcriptional start site. Competition for binding to the overlapping H-NS/ToxT binding sites was observed in gel mobility shift assays, where ToxT was found to displace H-NS from the ctx promoter region. In addition, regulatory differences between the ctx and tcpA promoters were examined. H-NS was found to have a higher relative binding affinity for the ctx promoter than for the tcpA promoter in vitro. In contrast to ToxT-dependent activation of the tcpA promoter, ToxT activation of ctx did not require the C-terminal domain of the ?-subunit of RNA polymerase. These findings demonstrate that transcriptional regulation of ctx and tcpA by H-NS and ToxT is mechanistically distinct, and this may lead to important differences in the expression of these coregulated genes.

| S-EPMC3028689 | biostudies-literature

Differential regulation of horizontally acquired and core genome genes by the bacterial modulator H-NS.

Project description:Horizontal acquisition of DNA by bacteria dramatically increases genetic diversity and hence successful bacterial colonization of several niches, including the human host. A relevant issue is how this newly acquired DNA interacts and integrates in the regulatory networks of the bacterial cell. The global modulator H-NS targets both core genome and HGT genes and silences gene expression in response to external stimuli such as osmolarity and temperature. Here we provide evidence that H-NS discriminates and differentially modulates core and HGT DNA. As an example of this, plasmid R27-encoded H-NS protein has evolved to selectively silence HGT genes and does not interfere with core genome regulation. In turn, differential regulation of both gene lineages by resident chromosomal H-NS requires a helper protein: the Hha protein. Tight silencing of HGT DNA is accomplished by H-NS-Hha complexes. In contrast, core genes are modulated by H-NS homoligomers. Remarkably, the presence of Hha-like proteins is restricted to the Enterobacteriaceae. In addition, conjugative plasmids encoding H-NS variants have hitherto been isolated only from members of the family. Thus, the H-NS system in enteric bacteria presents unique evolutionary features. The capacity to selectively discriminate between core and HGT DNA may help to maintain horizontally transmitted DNA in silent form and may give these bacteria a competitive advantage in adapting to new environments, including host colonization.

| S-EPMC2686267 | biostudies-literature

ToxR Antagonizes H-NS Regulation of Horizontally Acquired Genes to Drive Host Colonization.

Project description:This SuperSeries is composed of the SubSeries listed below.

2016-03-23 | GSE72474 | GEO

ToxR Antagonizes H-NS Regulation of Horizontally Acquired Genes to Drive Host Colonization.

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-03-23 | E-GEOD-72474 | biostudies-arrayexpress