The <i>hokW-sokW</i> Locus Encodes a Type I Toxin–Antitoxin System That Facilitates the Release of Lysogenic Sp5 Phage in Enterohemorrhagic <i>Escherichia coli</i> O157
The toxin-antitoxin (TA) genetic modules control various bacterial events, such as plasmid maintenance, persister cell formation, and phage defense. They also exist in mobile genetic elements, including prophages; however, their physiological roles remain poorly understood. Here, we demonstrate that...
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| Autores principales: | , , , |
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| Formato: | article |
| Lenguaje: | EN |
| Publicado: |
MDPI AG
2021
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| Materias: | |
| Acceso en línea: | https://doaj.org/article/e17afaa5891843469b9e06e86380412c |
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| Sumario: | The toxin-antitoxin (TA) genetic modules control various bacterial events, such as plasmid maintenance, persister cell formation, and phage defense. They also exist in mobile genetic elements, including prophages; however, their physiological roles remain poorly understood. Here, we demonstrate that <i>hokW-sokW</i>, a putative TA locus encoded in Sakai prophage 5 (Sp5) in enterohemorrhagic <i>Escherichia coli</i> O157: H7 Sakai strain, functions as a type I TA system. Bacterial growth assays showed that the antitoxic activity of <i>sokW</i> RNA against HokW toxin partially requires an endoribonuclease, RNase III, and an RNA chaperone, Hfq. We also demonstrated that <i>hokW-sokW</i> assists Sp5-mediated lysis of <i>E. coli</i> cells when prophage induction is promoted by the DNA-damaging agent mitomycin C (MMC). We found that MMC treatment diminished <i>sokW</i> RNA and increased both the expression level and inner membrane localization of HokW in a RecA-dependent manner. Remarkably, the number of released Sp5 phages decreased by half in the absence of <i>hokW-sokW</i>. These results suggest that <i>hokW-sokW</i> plays a novel role as a TA system that facilitates the release of Sp5 phage progeny through <i>E. coli</i> lysis. |
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