Dr Abbie Kelly abigail.kelly@durham.ac.uk
Technical Manager
Toxin–antitoxin systems as mediators of phage defence and the implications for abortive infection
Kelly, A.; Arrowsmith, T.J.; Went, S.C.; Blower, T.R.
Authors
T.J. Arrowsmith
S.C. Went
Professor Tim Blower timothy.blower@durham.ac.uk
Professor
Abstract
Bacteria have evolved a broad range of defence mechanisms to protect against infection by their viral parasites, bacteriophages (phages). Toxin–antitoxin (TA) systems are small loci found throughout bacteria and archaea that in some cases provide phage defence. The recent explosion in phage defence system discovery has identified multiple novel TA systems with antiphage activity. Due to inherent toxicity, TA systems are thought to mediate abortive infection (Abi), wherein the host cell dies in response to phage infection, removing the phage, and protecting clonal siblings. Recent studies, however, have uncovered molecular mechanisms by which TA systems are activated by phages, how they mediate toxicity, and how phages escape the defences. These new models reveal dazzling complexity in phage–host interactions and provide further evidence that TA systems do not in all cases inherently perform classic Abi, suggesting an evolved conceptual definition is required.
Citation
Kelly, A., Arrowsmith, T., Went, S., & Blower, T. (2023). Toxin–antitoxin systems as mediators of phage defence and the implications for abortive infection. Current Opinion in Microbiology, 73, Article 102293. https://doi.org/10.1016/j.mib.2023.102293
Journal Article Type | Article |
---|---|
Acceptance Date | Feb 24, 2023 |
Online Publication Date | Mar 21, 2023 |
Publication Date | 2023-06 |
Deposit Date | Mar 22, 2023 |
Publicly Available Date | Mar 23, 2023 |
Journal | Current Opinion in Microbiology |
Print ISSN | 1369-5274 |
Publisher | Elsevier |
Peer Reviewed | Peer Reviewed |
Volume | 73 |
Article Number | 102293 |
DOI | https://doi.org/10.1016/j.mib.2023.102293 |
Public URL | https://durham-repository.worktribe.com/output/1176720 |
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Publisher Licence URL
http://creativecommons.org/licenses/by/4.0/
Copyright Statement
Crown Copyright © 2023 Published by Elsevier Ltd.
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