ArticleGenome biology and evolution2020
Two Lineages of Pseudomonas aeruginosa Filamentous Phages: Structural Uniformity over Integration Preferences.
Article in Genome biology and evolution, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed.
- Intra-strain genomic microevolution and phage resistance inMicrobiology spectrum · 2026Article
- Disrupting phage liquid crystalline droplets restores antibiotic susceptibility in Pseudomonas aeruginosa biofilms.PLoS biology · 2026Article
- Jumbo phage-mediated transduction of genomic islands.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Metagenome-inspired libraries to engineer phage M13 for targeted killing of Gram-negative bacterial species.Nucleic acids research · 2025Article
- New Pseudomonas infections drive Pf phage transmission in CF airways.JCI insight · 2025Article
- Study of the probability of resistance to phage infection in a collection of clinical isolates ofMicrobiology spectrum · 2025Article
- Inovirus-Encoded Peptides Induce Specific Toxicity inViruses · 2025Article
- Article
- Engineered Bacteriophage-Polymer Nanoassemblies for Treatment of Wound Biofilm Infections.ACS nano · 2024Article
- Review
- VIBES: a workflow for annotating and visualizing viral sequences integrated into bacterial genomes.NAR genomics and bioinformatics · 2024Article
- Pf bacteriophages hinder sputum antibiotic diffusion via electrostatic binding.Science advances · 2024Article
- Targeted deletion of Pf prophages from diverseJournal of bacteriology · 2024Article
- Pf bacteriophages hinder sputum antibiotic diffusion via electrostatic binding.bioRxiv : the preprint server for biology · 2024Article
- Adjuvanted Vaccine Induces Functional Antibodies againstVaccines · 2024Article
- The Inovirus Pf4 Triggers Antiviral Responses and Disrupts the Proliferation of Airway Basal Epithelial Cells.Viruses · 2024Article
- Divergent molecular strategies drive evolutionary adaptation to competitive fitness in biofilm formation.The ISME journal · 2024Article
- Article
- Inhibition of PQS signaling by the Pf bacteriophage protein PfsE enhances viral replication in Pseudomonas aeruginosa.Molecular microbiology · 2024Article
- The dataset on the draft whole-genome sequences of twoData in brief · 2023Article
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6 authors.
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Abstract
Pseudomonas aeruginosa filamentous (Pf) bacteriophages are important factors contributing to the pathogenicity of this opportunistic bacterium, including biofilm formation and suppression of bacterial phagocytosis by macrophages. In addition, the capacity of Pf phages to form liquid crystal structures and their high negative charge density makes them potent sequesters of cationic antibacterial agents, such as aminoglycoside antibiotics or host antimicrobial peptides. Therefore, Pf phages have been proposed as a potential biomarker for risk of antibiotic resistance development. The majority of studies describing biological functions of Pf viruses have been performed with only three of them: Pf1, Pf4, and Pf5. However, our analysis revealed that Pf phages exist as two evolutionary lineages (I and II), characterized by substantially different structural/morphogenesis properties, despite sharing the same integration sites in the host chromosomes. All aforementioned model Pf phages are members of the lineage I. Hence, it is reasonable to speculate that their interactions with P. aeruginosa and impact on its pathogenicity may be not completely extrapolated to the lineage II members. Furthermore, in order to organize the present numerical nomenclature of Pf phages, we propose a more informative approach based on the insertion sites, that is, Pf-tRNA-Gly, -Met, -Sec, -tmRNA, and -DR (direct repeats), which are fully compatible with one of five types of tyrosine integrases/recombinases XerC/D carried by these viruses. Finally, we discuss possible evolutionary mechanisms behind this division and consequences from the perspective of virus-virus, virus-bacterium, and virus-human interactions.
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