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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Main Authors: Kosuke Takada, Kotone Hama, Takaomi Sasaki, Yuichi Otsuka
Format: Article
Language:English
Published: MDPI AG 2021-11-01
Series:Toxins
Subjects:
Online Access:https://www.mdpi.com/2072-6651/13/11/796
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author Kosuke Takada
Kotone Hama
Takaomi Sasaki
Yuichi Otsuka
author_facet Kosuke Takada
Kotone Hama
Takaomi Sasaki
Yuichi Otsuka
author_sort Kosuke Takada
collection DOAJ
description 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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spelling doaj.art-e17afaa5891843469b9e06e86380412c2023-11-23T01:49:15ZengMDPI AGToxins2072-66512021-11-01131179610.3390/toxins13110796The <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> O157Kosuke Takada0Kotone Hama1Takaomi Sasaki2Yuichi Otsuka3Department of Biochemistry and Molecular Biology, Graduate School of Science and Engineering, Saitama University, 255 Shimo-Okubo, Sakura-Ku, Saitama 338-8570, JapanDepartment of Biochemistry and Molecular Biology, Graduate School of Science and Engineering, Saitama University, 255 Shimo-Okubo, Sakura-Ku, Saitama 338-8570, JapanDepartment of Biochemistry and Molecular Biology, Graduate School of Science and Engineering, Saitama University, 255 Shimo-Okubo, Sakura-Ku, Saitama 338-8570, JapanDepartment of Biochemistry and Molecular Biology, Graduate School of Science and Engineering, Saitama University, 255 Shimo-Okubo, Sakura-Ku, Saitama 338-8570, JapanThe 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.https://www.mdpi.com/2072-6651/13/11/796bacteriophage<i>Escherichia coli</i>toxin–antitoxin systemprophage induction
spellingShingle Kosuke Takada
Kotone Hama
Takaomi Sasaki
Yuichi Otsuka
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
Toxins
bacteriophage
<i>Escherichia coli</i>
toxin–antitoxin system
prophage induction
title 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
title_full 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
title_fullStr 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
title_full_unstemmed 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
title_short 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
title_sort 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
topic bacteriophage
<i>Escherichia coli</i>
toxin–antitoxin system
prophage induction
url https://www.mdpi.com/2072-6651/13/11/796
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