ArticleNucleic acids research2022
A phage weaponizes a satellite recombinase to subvert viral restriction.
Article in Nucleic acids research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
- Article
- The Multi-dimensional Mechanisms and Transformation Prospects of the Intratumoral Microbiota-Arginine Metabolism Axis in Tumor Progression and Immune Regulation.International journal of medical sciences · 2026Review
- Lineage-specific defence systems of pandemicPhilosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025Review
- Why do bacteria accumulate antiphage defence systems?Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025Review
- Genetics, ecology and evolution of phage satellites.Nature reviews. Microbiology · 2025Review
- A phage satellite manipulates the viral DNA packaging motor to inhibit phage and promote satellite spread.Nucleic acids research · 2024Article
- A phage satellite manipulates the viral DNA packaging motor to inhibit phage and promote satellite spread.bioRxiv : the preprint server for biology · 2024Article
- AeLife · 2024Article
- Genomic analysis of hyperparasitic viruses associated with entomopoxviruses.Virus evolution · 2024Article
- Sporadic phage defense in epidemicbioRxiv : the preprint server for biology · 2023Article
- AbioRxiv : the preprint server for biology · 2023Article
- Nuclease genes occupy boundaries of genetic exchange between bacteriophages.NAR genomics and bioinformatics · 2023Article
- Nuclease genes occupy boundaries of genetic exchange between bacteriophages.bioRxiv : the preprint server for biology · 2023Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Bacteria can acquire mobile genetic elements (MGEs) to combat infection by viruses (phages). Satellite viruses, including the PLEs (phage-inducible chromosomal island-like elements) in epidemic Vibrio cholerae, are MGEs that restrict phage replication to the benefit of their host bacterium. PLEs parasitize the lytic phage ICP1, unleashing multiple mechanisms to restrict phage replication and promote their own spread. In the arms race against PLE, ICP1 uses nucleases, including CRISPR-Cas, to destroy PLE's genome during infection. However, through an unknown CRISPR-independent mechanism, specific ICP1 isolates subvert restriction by PLE. Here, we discover ICP1-encoded Adi that counteracts PLE by exploiting the PLE's large serine recombinase (LSR), which normally mobilizes PLE in response to ICP1 infection. Unlike previously characterized ICP1-encoded anti-PLE mechanisms, Adi is not a nuclease itself but instead appears to modulate the activity of the LSR to promote destructive nuclease activity at the LSR's specific attachment site, attP. The PLE LSR, its catalytic activity, and attP are additionally sufficient to sensitize a PLE encoding a resistant variant of the recombination module to Adi activity. This work highlights a unique type of adaptation arising from inter-genome conflicts, in which the intended activity of a protein can be weaponized to overcome the antagonizing genome.
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Registered trials
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