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Abiotic influence on phage resistance evolution

ABSTRACT: Abiotic influence on phage resistance evolution

PROVIDER: PRJEB51326 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR9714360_1.fastq.gz	Fastqsanger.gz
	ERR9714360_2.fastq.gz	Fastqsanger.gz
	ERR9714370_1.fastq.gz	Fastqsanger.gz
	ERR9714370_2.fastq.gz	Fastqsanger.gz
	ERR9714361_1.fastq.gz	Fastqsanger.gz

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Influence of the aminoglycoside antibiotic apramycin on host and phage DNA transcription during infection of S. venezuelae ATCC 10712 with phage Alderaan

Project description:Bacterial populations face the constant threat of viral predation exerted by bacteriophages (or phages). In response, bacteria have evolved a wide range of defense mechanisms against phage challenges. Here, we show that aminoglycosides, a well-known class of antibiotics produced by Streptomyces, are potent inhibitors of phage infection. We observed a broad phage inhibition by aminoglycosides. We demonstrate that aminoglycosides do not prevent the injection of phage DNA into bacterial cells but instead block an early step of the viral life cycle. In this context, we used RNA sequencing of S. venezuelae cells infected with phage Alderaan to comparatively investigate the influence of apramycin on phage DNA tanscription at two different time points after inital infection.

2021-04-30 | GSE171784 | GEO

The transcriptional program of Staphylococcus aureus phage K is affected by a host rpoC mutation that confers phage K resistance

Project description:To better understand host/phage interactions and the genetic bases of phage resistance in a model system relevant to potential phage therapy, we isolated several spontaneous mutants of the USA300 S. aureus clinical isolate NRS384 that were resistant to phage K. Six of these had a single missense mutation in the host rpoC gene, which encodes the RNA polymerase beta prime subunit. To examine the hypothesis that the mutations in the host RNA polymerase affect the transcription of phage genes, we performed RNA-seq analysis on total RNA samples collected from NRS384 wild-type (WT) and rpoC G17D mutant cultures infected with phage K, at different time points after infection. Infection of the WT host led to a steady increase of phage transcription relative to the host. Our analysis allowed us to define different early, middle, and late phage genes based on their temporal expression patterns and group them into transcriptional units. Predicted promoter sequences defined by conserved -35, -10, and in some cases extended -10 elements were found upstream of early and middle genes. However, sequences upstream of late genes did not contain clear, complete, canonical promoter sequences, suggesting that factors in addition to host RNA polymerase are required for their regulated expression. Infection of the rpoC G17D mutant host led to a transcriptional pattern that was similar to the WT at early time points. However, beginning at 20 minutes after infection, transcription of late genes (such as phage structural genes and host lysis genes) was severely reduced. Our data indicate that the rpoCG17D mutation prevents the expression of phage late genes, resulting in a failed infection cycle for phage K. In addition to illuminating the global transcriptional landscape of phage K throughout the infection cycle, these studies can inform our investigations into the bases of phage K’s control of its transcriptional program as well as mechanisms of phage resistance.

2024-10-09 | GSE253516 | GEO

The lactococcal phage p2 protein ORF47 impedes Lactococcus lactis MG1363 resistance to phage infection

Project description:The lactococcal phage p2 is a model for studying the Skunavirus genus, the most prevalent group of phages in cheese factories worldwide. It infects L. lactis MG1363, a model strain for the study of Gram-positive bacteria. The structural proteins of phage p2 have been thoroughly described. However, most of its non-structural proteins are still uncharacterized. Here, we developed an integrative approach, making use of structural biology, genomics, physiology, and proteomics to provide insights into the function of ORF47, the most conserved non-structural protein of unknown function among the Skunavirus genus. We found this small phage protein to have a major impact on the bacterial proteome and to be important to prevent bacterial resistance to phage infection.

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Parallel evolution of phage resistance in vitro and in vivo in Pseudomonas aeruginosa.

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K5 capsule and lipopolysaccharide are important in resistance to T4 phage attack in probiotic E. coli strain Nissle 1917

Project description:Rapidly growing antibiotic resistance among gastrointestinal pathogens, and the ability of antibiotics to induce the virulence of these pathogens makes it increasingly difficult to rely on antibiotics to treat gastrointestinal infections. The probiotic E. coli strain Nissle 1917 (EcN) is the active component of the pharmaceutical preparation Mutaflor® and has been successfully used in the treatment of gastrointestinal disorders. Gut bacteriophages are dominant players in maintaining the microbial homeostasis in the gut, however, their interaction with incoming probiotic bacteria remains to be at conception. The presence of bacteriophages in the gut makes it inevitable for any probiotic bacteria to be phage resistant, in order to survive and successfully colonize the gut. This study addresses the phage resistance of EcN, specifically against lytic T4 phage infection. From various experiments we could show that i) EcN is resistant towards T4 phage infection, ii) EcN’s K5 polysaccharide capsule plays a crucial role in T4 phage resistance and iii) EcN’s lipopolysaccharide (LPS) inactivates T4 phages and notably, treatment with the antibiotic polymyxin B which neutralizes the LPS destroyed the phage inactivation ability of isolated LPS from EcN. Our results further indicate that N-acetylglucosamine at the distal end of O6 antigen in EcN’s LPS could be the interacting partner with T4 phages. From our findings, we have reported for the first time, the role of EcN’s K5 capsule and LPS in its defense against T4 phages. In addition, by inactivating the T4 phages, EcN also protects E. coli K-12 strains from phage infection in tri-culture experiments. The combination of the identified properties is not found in other tested commensal E. coli strains. Furthermore, our research highlights phage resistance as an additional safety feature of EcN, a clinically successful probiotic E. coli strain.

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2019-03-31 | GSE126873 | GEO

Phage Diversity

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Genomic and gene-expression comparisons among phage-resistant type-IV pilus mutants of Pseudomonas syringae pathovar phaseolicola

Project description:Pseudomonas syringae pv. phaseolicola (Pph) is a significant bacterial pathogen of agricultural crops, and phage Î¦6 and other members of the dsRNA virus family Cystoviridae undergo lytic (virulent) infection of Pph, using the type IV pilus as the initial site of cellular attachment. Despite the popularity of Pph/phage Î¦6 as a model system in evolutionary biology, Pph resistance to phage Î¦6 remains poorly characterized. To investigate differences between phage Î¦6 resistant Pseudomonas syringae pathovar phaseolicola strains, we performed expression analysis of super and non piliated strains of Pseudomonas syringae to determine the genetic cause of resistance to viral infection.

2016-03-15 | E-MTAB-4053 | biostudies-arrayexpress

Comparative transcriptomics reveals a conserved Bacterial Adaptive Phage Response (BAPR) to viral predation

Project description:Intrinsic and acquired defenses against bacteriophages, including Restriction/Modification, CRISPR/Cas, and Toxin/Anti-toxin systems have been intensely studied, with profound scientific impacts. However, adaptive defenses against phage infection analogous to adaptive resistance to antimicrobials have yet to be described. To identify such mechanisms, we applied an RNAseq-based, comparative transcriptomics approach in different \textit{Pseudomonas aeruginosa} strains after independent infection by a set of divergent virulent bacteriophages. A common host-mediated adaptive stress response to phages was identified that includes the Pseudomonas Quinolone Signal, through which infected cells inform their neighbors of infection, and what may be a resistance mechanism that functions by reducing infection vigor. With host transcriptional machinery left intact, we also observe phage-mediated differential expression caused by phage-specific stresses and molecular mechanisms. These responses suggest the presence of a conserved Bacterial Adaptive Phage Response mechanism as a novel type of host defense mechanism, and which may explain transient forms of phage persistence.

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