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

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

PROVIDER: PRJNA1053818 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27238711_1.fastq.gz	Fastqsanger.gz
	SRR27238711_2.fastq.gz	Fastqsanger.gz
	SRR27238712_1.fastq.gz	Fastqsanger.gz
	SRR27238712_2.fastq.gz	Fastqsanger.gz
	SRR27238713_1.fastq.gz	Fastqsanger.gz

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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]

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

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

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

2024-02-09 | GSE250408 | GEO

Horizontally-acquired AmpC (FOX-4) in Pseudomonas aeruginosa

Project description:Emergence of resistance to novel β-lactam β-lactamase inhibitor combinations due to horizontally-acquired AmpC (FOX-4) in Pseudomonas aeruginosa

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Optogenetic control of the horizontally acquired region A reveal its importance to prevent stuck fermentations in a wine yeast

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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

The ancestral SgrS RNA discriminates horizontally acquired Salmonella mRNAs through a single G-U wobble pair

Project description:SgrS RNA is a model for the large class of Hfq-associated small RNAs that act to post-transcriptionally regulate bacterial mRNAs. The function of SgrS is well-characterized in non-pathogenic Escherichia coli where it was originally shown to counteract glucose-phosphate stress by acting as a repressor of ptsG mRNA which encodes the major glucose transporter. We have discovered new SgrS targets in Salmonella Typhimurium, a pathogen related to E. coli, which recently acquired a quarter of all genes by horizontal gene transfer. We demonstrate that the conserved short seed region of SgrS that recognizes ptsG was recruited to target the Salmonella-specific sopD mRNA of a secreted virulence protein. The SgrS-sopD interaction is exceptionally selective; we find that sopD2 mRNA whose gene arose from sopD duplication during Salmonella evolution, is deaf to SgrS owing to a non-productive G:U pair in the potential SgrS-sopD2 RNA duplex versus G:C in SgrS-sopD. In other words, SgrS discriminates the two virulence factor mRNAs at the level of a single hydrogen bond. Our study suggests that bacterial pathogens employ their large suites of conserved Hfq-associated regulators to integrate horizontally acquired genes into existing post-transcriptional networks, just as conserved transcription factors are recruited to tame foreign genes at the DNA level. The results graphically illustrate the importance of the seed regions of bacterial small RNAs to select new targets with high fidelity, and argue that target predictions must consider all-or-none decisions by individual seed nucleotides.

2012-01-20 | GSE34851 | GEO

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