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Transcriptional response of Pseudomonas aeruginosa PA3 to its phage gene product gp68

ABSTRACT: Explore the genome-scale influence of PA3 phage gene product gp68 on Pseudomonas aeruginosa PA3

ORGANISM(S): Pseudomonas aeruginosa

PROVIDER: GSE126873 | GEO | 2019/03/31

REPOSITORIES: GEO

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Transcriptional response of Pseudomonas aeruginosa PA3 to its phage gene product gp68

Project description:Transcriptional response of Pseudomonas aeruginosa PA3 to its phage gene product gp68

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The phage-encoded protein PIT2 impacts bacterial quorum sensing in Pseudomonas aeruginosa by direct interaction with LasR

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Transcriptomic and Metabolomics Profiling of Phage–Host Interactions between Phage PaP1 and Pseudomonas aeruginosa

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The phage-encoded PIT4 protein impacts the Pseudomonas aeruginosa type IV pili by affecting different two-component systems

Project description:Two component systems (TCSs) control a large proportion of virulence factors in Pseudomonas aeruginosa. Yet, investigations on inhibitors of regulatory pathways of TCS remain scare, despite their potential in anti-virulence strategies. This work encompasses the working mechanism of PIT4, a protein derived from the lytic P. aeruginosa phage LSL4. This viral protein inhibits bacterial motility and in particular twitching motility, while reducing the virulence of P. aeruginosa towards HeLa cells. Via differential gene expression and a yeast two-hybrid screen, PIT4 was shown to interact with components of different two component systems. In one-on-one interaction assays, it was confirmed that PIT4 interacts with the histidine kinases FleS, PilS and PA2882, through interaction with the histidine kinase domain. As such, this work highlights the potential of previously unknown phage proteins in virulence regulation of multidrug resistant pathogens that might be exploited for anti-virulence strategies and biotechnological applications.

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Pseudomonas aeruginosa lasR QS network promotes phage infection by regulating the biosynthesis of LPS and type IV pili by regulating the biosynthesis of LPS and type IV pili

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Project description:Pseudomonas aeruginosa bacteriophage PhiKZ is the type representative of the M-bM-^@M-^XgiantM-bM-^@M-^Y phage genus with unusually large virions and genomes. By unraveling the transcriptional map of the 280 kb genome to single-nucleotide resolution, we show that it encodes 369 genes organized in 134 operons, 20% more than originally annotated. Early transcription is initiated from 28 highly conserved AT-rich promoters distributed over the PhiKZ genome, all located on the same strand. Transcription of middle and late genes is dependent on protein synthesis and mediated by very poorly conserved middle (6) and late (16) promoters. As a result of massive PhiKZ transcription, halfway through infection only 1.5% of all mRNAs in the infected cell remain bacterial. Unique to PhiKZ is its ability to complete its infection in complete absence of bacterial RNA polymerase (RNAP) enzyme activity. Its transcription is performed by the consecutive action of two PhiKZ-encoded, non-canonical RNAPs, one of which is packed within the virion. This unique, rifampicin-resistant transcriptional machinery is conserved among giant viruses, seems to function without auxiliary factors and might have its origin preceding the split between Gram-positive and Gram-negative bacteria. Construction of transcription maps for the PhiKZ phage and analysis of differential expression of host and phage genes using RNA-Seq data from samples taken in duplicate at 0, 5, 10, 15, and 35 minutes into infection.

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Proteomic analyses of Pseudomonas infected with giant phage PhiKZ

Project description:Preliminary analyses of Pseudomonas aeruginosa cells infected with phage PhiKZ and a control at 20 minutes post infection.

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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

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