Antagonistic interactions between phage and host factors control arbitrium lysis-lysogeny decision.

Zamora-Caballero, Sara, Chmielowska, Cora, Quiles-Puchalt, Nuria, Brady, Aisling ORCID: 0000-0001-5177-4813, Del Sol, Francisca Gallego, Mancheño-Bonillo, Javier, Felipe-Ruíz, Alonso, Meijer, Wilfried JJ, Penadés, José R and Marina, Alberto (2024) Antagonistic interactions between phage and host factors control arbitrium lysis-lysogeny decision. Nature microbiology, 9 (1). pp. 161-172.

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Official URL: http://dx.doi.org/10.1038/s41564-023-01550-4

Abstract

Phages can use a small-molecule communication arbitrium system to coordinate lysis-lysogeny decisions, but the underlying mechanism remains unknown. Here we determined that the arbitrium system in Bacillus subtilis phage phi3T modulates the bacterial toxin-antitoxin system MazE-MazF to regulate the phage life cycle. We show that phi3T expresses AimX and YosL, which bind to and inactivate MazF. AimX also inhibits the function of phi3T_93, a protein that promotes lysogeny by binding to MazE and releasing MazF. Overall, these mutually exclusive interactions promote the lytic cycle of the phage. After several rounds of infection, the phage-encoded AimP peptide accumulates intracellularly and inactivates the phage antiterminator AimR, a process that eliminates aimX expression from the aimP promoter. Therefore, when AimP increases, MazF activity promotes reversion back to lysogeny, since AimX is absent. Altogether, our study reveals the evolutionary strategy used by arbitrium to control lysis-lysogeny by domesticating and fine-tuning a phage-defence mechanism.

Item Type:	Article
Uncontrolled Keywords:	Bacillus Phages, Peptides, Lysogeny, Cell Death
Divisions:	Faculty of Health and Life Sciences Faculty of Health and Life Sciences > Institute of Infection, Veterinary and Ecological Sciences
Depositing User:	Symplectic Admin
Date Deposited:	30 Jan 2024 09:53
Last Modified:	30 Jan 2024 10:55
DOI:	10.1038/s41564-023-01550-4
Open Access URL:	https://doi.org/10.1038/s41564-023-01550-4
Related URLs:	Author Publisher
URI:	https://livrepository.liverpool.ac.uk/id/eprint/3178067