Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

H-NS-like proteins in Pseudomonas aeruginosa coordinately silence intragenic transcription [RNA-seq]

ABSTRACT: The H-NS-like proteins MvaT and MvaU act coordinately as global repressors in Pseudomonas aeruginosa by binding to AT-rich regions of the chromosome. Although cells can tolerate the loss of either protein, identifying their combined regulatory effects has been challenging because the loss of both proteins is lethal due to induction of prophage Pf4 and subsequent superinfection of the cell. In other bacteria, H-NS promotes cellular fitness by inhibiting intragenic transcription from AT-rich target regions, preventing them from sequestering RNA polymerase; however, it is not known if whether MvaT and MvaU function similarly. Here we utilize a parental strain that cannot be infected by Pf4 phage to define the collective MvaT and MvaU regulon and demonstrate that the combined loss of both MvaT and MvaU leads to increased intragenic transcription from loci directly controlled by these proteins. We further show that the loss of MvaT and MvaU leads to a striking redistribution of RNA polymerase containing σ70 to genomic regions vacated by these proteins. Our findings suggest that the ability of H-NS-like proteins to repress intragenic transcription is a universal function of these proteins and point to a second mechanism by which MvaT and MvaU may contribute to the growth of P. aeruginosa.

ORGANISM(S): Pseudomonas aeruginosa PAO1

PROVIDER: GSE155023 | GEO | 2020/12/23

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

H-NS-like proteins in Pseudomonas aeruginosa coordinately silence intragenic transcription [ChIP-seq]

Project description:The H-NS-like proteins MvaT and MvaU act coordinately as global repressors in Pseudomonas aeruginosa by binding to AT-rich regions of the chromosome. Although cells can tolerate the loss of either protein, identifying their combined regulatory effects has been challenging because the loss of both proteins is lethal due to induction of prophage Pf4 and subsequent superinfection of the cell. In other bacteria, H-NS promotes cellular fitness by inhibiting intragenic transcription from AT-rich target regions, preventing them from sequestering RNA polymerase; however, it is not known if whether MvaT and MvaU function similarly. Here we utilize a parental strain that cannot be infected by Pf4 phage to define the collective MvaT and MvaU regulon and demonstrate that the combined loss of both MvaT and MvaU leads to increased intragenic transcription from loci directly controlled by these proteins. We further show that the loss of MvaT and MvaU leads to a striking redistribution of RNA polymerase containing σ70 to genomic regions vacated by these proteins. Our findings suggest that the ability of H-NS-like proteins to repress intragenic transcription is a universal function of these proteins and point to a second mechanism by which MvaT and MvaU may contribute to the growth of P. aeruginosa.

2020-12-23 | GSE155024 | GEO

Transcriptome analysis of mvaT and mvaU double knockout mutant of Pseudomonas aeruginosa PAO1

Project description:MvaT and MvaU are two redundant xenogeneic silencing proteins of the H-NS family in Pseudomonas aeruginosa. Previous studies to investigate the physiological consequences of mvaT and mvaU depletion were hampered by activation of Pf4 prophage in the resulting mutants. In this study, an mvaT mvaU double knockout mutant (PAO△TU) was constructed in a strain of PAO1 (Δpf4) devoid of the Pf4 prophage on the chromosome.Transcriptome analysis by GeneChip (Affymetrix) revealed that over 227 genes were found up-regulated in PAO△TU, including several multi-gene loci for type III and type VI protein secretion systems, O-antigen, exopolysaccharide, pili assembly, and many others of unknown functions.

2019-08-08 | GSE135506 | GEO

Pf4 infection alters P. aeruginosa virulence

Project description:Pf4 is a filamentous bacteriophage integrated as a prophage into the genome of Pseudomonas aeruginosa PAO1. Pf4 virions can be produced without killing P. aeruginosa. Cell lysis can however occur during superinfection when Pf virions successfully infect a host lysogenized by a Pf superinfective variant. We have previously shown that infection of P. aeruginosa PAO1 with a superinfective Pf4 variant led to abolish twitching motility and to alter biofilm’s architecture. More precisely, the cells embedded into the biofilm were showing for most of them a filamentous morphology, that could be related to the activation of the cell envelope stress response involving both the AlgU and SigX extra cytoplasmic function sigma factors. Herein, we show that Pf4 variant-infection resulted also into a drastic dysregulation of 3,360 genes representing about 58% of P. aeruginosa’s genome, of which about 43% of the virulence factors encoding genes showing a down-regulation. Accordingly, Pf4 variant infection (termed Pf4*) causes in vivo reduction of P. aeruginosa virulence, decreased production of N-acyl-homoserine lactones and 2-alkyl-4-quinolones quorum sensing molecules, and related virulence factors, such as pyocyanin, elastase, and pyoverdine. In addition to virulence encoding genes, expression of genes involved in metabolism, including energy generation and iron homeostasis, was affected, suggesting further relationships between virulence and central metabolism. Altogether, these data suggest that Pf4 phage variant infection results in complex networks dysregulations, leading to reducing acute virulence in P. aeruginosa. This work contributes to the comprehension of the bacterial response to filamentous phage infection.

2022-07-05 | GSE201738 | GEO

The repressor C protein, Pf4r, controls superinfection of Pseudomonas aeruginosa PAO1 by the Pf4 filamentous phage and regulates host gene expression

Project description:It has been shown that the filamentous phage, Pf4, plays an important role in biofilm development, stress tolerance, genetic variant formation and virulence in Pseudomonas aeruginosa PAO1. These behaviours are linked to the appearance of superinfective phage variants. Here, we have investigated the molecular mechanism of superinfection as well as how the Pf4 phage can control host gene expression to modulate host behaviours. Pf4 exists as a prophage in PAO1 and encodes a homolog of the P2 phage repressor C. Through a combination of molecular techniques, ChIPseq and transcriptomic analyses, we show that repressor C (Pf4r) is the minimal factor for immunity against reinfection by Pf4 possibly through Pf4r binding to its putative promoter region, and that Pf4r also functions as a transcriptional regulator for expression of host genes. A binding motif for Pf4r was also identified. In wild type P. aeruginosa and Pfr4 complemented Pf4 deficient mutant strains, virulence factor related genes including phenazine and type VI secretion system effectors were upregulated, potentially explaining the reduced virulence of Pf4-deficient P. aeruginosa PAO1. X-ray crystal structure analysis shows that Pf4r forms symmetric homo-dimers homologous to the E.coli bacteriophage P2 RepC protein. A mutation associated with the superinfective Pf4r variant, found at the dimer interface, suggests dimer formation may be disrupted, which derepresses phage replication. This is supported by MALS analysis where the Pf4r* protein only shows monomer formation. Collectively, these data suggest the mechanism by which filamentous phages play such an important role in P. aeruginosa biofilm development.

2021-01-31 | GSE154459 | GEO

H-NS-like proteins in Pseudomonas aeruginosa coordinately silence intragenic transcription

Project description:H-NS-like proteins in Pseudomonas aeruginosa coordinately silence intragenic transcription

| PRJNA648174 | ENA

H-NS-like proteins in Pseudomonas aeruginosa coordinately silence intragenic transcription [ChIP-seq]

Project description:H-NS-like proteins in Pseudomonas aeruginosa coordinately silence intragenic transcription [ChIP-seq]

| PRJNA648196 | ENA

H-NS-like proteins in Pseudomonas aeruginosa coordinately silence intragenic transcription [RNA-seq]

Project description:H-NS-like proteins in Pseudomonas aeruginosa coordinately silence intragenic transcription [RNA-seq]

| PRJNA648195 | ENA

MvaT family proteins encoded on IncP-7 plasmid pCAR1 and the host chromosome regulate host transcriptome cooperatively but differently (pCAR1)

Project description:MvaT proteins are recognized as a member of H-NS family proteins in pseudomonads. IncP-7 conjugative plasmid pCAR1, which was originally found in Pseudomonas resinovorans, carries an mvaT homologous gene, pmr. In Pseudomonas putida KT2440 bearing pCAR1, it was previously reported that pmr and chromosomally-encoded homologous genes, turA and turB, are majorly transcribed, and that Pmr interacts with TurA and TurB in vitro (Yun et al. J. Bacteriol. 192:4720-4731, 2010). In the present study, we clarified how the three MvaT proteins regulate the transcriptome of P. putida KT2440(pCAR1). Modified ChIP-chip analyses suggested that the binding sites of Pmr, TurA, and TurB in P. putida KT2440(pCAR1) genome were almost identical; nevertheless, transcriptome analyses using deletion mutants of each MvaT protein gene at the log and early-stationary growth phases clearly suggested that their regulons were different with one another. Especially, significant dissimilarity of regulons was found between Pmr and other two proteins. Transcriptions of the larger number of genes were affected by Pmr deletion at the early-stationary phase than at the log phase, suggesting that Pmr minimizes the pCAR1 effects on host fitness more effectively at the early-stationary phase. On the other hand, similarity found between the regulons of TurA and TurB implied that they may have complementary roles as global transcriptional regulators in response to the plasmid carriage. ChIP-chip: Pseudomonas putida KT2440 harboring plasmid pCAR1 cells were ChIPed with His-tag (C-terminus of each MvaT homologs) and compared with input control. Transcriptome analysis: pCAR1 RNA maps of mvaT deletion mutants were compared with those of wild-type cells.

2015-09-03 | E-GEOD-72638 | biostudies-arrayexpress

MvaT family proteins encoded on IncP-7 plasmid pCAR1 and the host chromosome regulate host transcriptome cooperatively but differently (KT2440)

Project description:MvaT proteins are recognized as a member of H-NS family proteins in pseudomonads. IncP-7 conjugative plasmid pCAR1, which was originally found in Pseudomonas resinovorans, carries an mvaT homologous gene, pmr. In Pseudomonas putida KT2440 bearing pCAR1, it was previously reported that pmr and chromosomally-encoded homologous genes, turA and turB, are majorly transcribed, and that Pmr interacts with TurA and TurB in vitro (Yun et al. J. Bacteriol. 192:4720-4731, 2010). In the present study, we clarified how the three MvaT proteins regulate the transcriptome of P. putida KT2440(pCAR1). Modified ChIP-chip analyses suggested that the binding sites of Pmr, TurA, and TurB in P. putida KT2440(pCAR1) genome were almost identical; nevertheless, transcriptome analyses using deletion mutants of each MvaT protein gene at the log and early-stationary growth phases clearly suggested that their regulons were different with one another. Especially, significant dissimilarity of regulons was found between Pmr and other two proteins. Transcriptions of the larger number of genes were affected by Pmr deletion at the early-stationary phase than at the log phase, suggesting that Pmr minimizes the pCAR1 effects on host fitness more effectively at the early-stationary phase. On the other hand, similarity found between the regulons of TurA and TurB implied that they may have complementary roles as global transcriptional regulators in response to the plasmid carriage. ChIP-chip: Pseudomonas putida KT2440 harboring plasmid pCAR1 cells were ChIPed with His-tag (C-terminus of each MvaT homologs) and compared with input control. Transcriptome analysis: Chromosomal RNA maps of mvaT deletion mutants were compared with those of wild-type cells.

2015-09-03 | E-GEOD-72637 | biostudies-arrayexpress

MvaT family proteins encoded on IncP-7 plasmid pCAR1 and the host chromosome regulate host transcriptome cooperatively but differently (pCAR1)

2015-09-03 | GSE72638 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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