Cyclic nucleotide signaling in phage defense and counter-defense
Abstract
Advances in our understanding of prokaryotic antiphage defense mechanisms in the past few years have revealed a multitude of new cyclic nucleotide signaling molecules that play a crucial role in switching infected cells into an antiviral state. Defense pathways including type III CRISPR (clustered regularly interspaced palindromic repeats), CBASS (cyclic nucleotide-based antiphage signaling system), PYCSAR (pyrimidine cyclase system for antiphage resistance), and Thoeris all use cyclic nucleotides as second messengers to activate a diverse range of effector proteins. These effectors typically degrade or disrupt key cellular components such as nucleic acids, membranes, or metabolites, slowing down viral replication kinetics at great cost to the infected cell. Mechanisms to manipulate the levels of cyclic nucleotides are employed by cells to regulate defense pathways and by viruses to subvert them. Here we review the discovery and mechanism of the key pathways, signaling molecules and effectors, parallels and differences between the systems, open questions, and prospects for future research in this area.
Citation
Athukoralage , J S & White , M F 2022 , ' Cyclic nucleotide signaling in phage defense and counter-defense ' , Annual Review of Virology , vol. 9 , pp. 451-468 . https://doi.org/10.1146/annurev-virology-100120-010228
Publication
Annual Review of Virology
Status
Peer reviewed
ISSN
2327-056XType
Journal article
Rights
Copyright © 2022 by Annual Reviews. This work is licensed under a Creative Commons Attribution 4.0 International License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. See credit lines of images or other third-party material in this article for license information.
Description
Work on cyclic nucleotide signaling in the authors’ lab is supported by the Biotechnology and Biological Sciences Research Council (ref. BB/S000313 and BB/T004789) and a European Research Council Advanced Grant (grant 101018608). J.S.A. is supported by a European Molecular Biology Organization long-term fellowship (ALTF 1201-2020).Collections
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