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...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: Kosuke Takada, Kotone Hama, Takaomi Sasaki, Yuichi Otsuka
Formato: article
Lenguaje:EN
Publicado: MDPI AG 2021
Materias:
R
Acceso en línea:https://doaj.org/article/e17afaa5891843469b9e06e86380412c
Etiquetas: Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
id oai:doaj.org-article:e17afaa5891843469b9e06e86380412c
record_format dspace
spelling oai:doaj.org-article:e17afaa5891843469b9e06e86380412c2021-11-25T19:08:54ZThe <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> O15710.3390/toxins131107962072-6651https://doaj.org/article/e17afaa5891843469b9e06e86380412c2021-11-01T00:00:00Zhttps://www.mdpi.com/2072-6651/13/11/796https://doaj.org/toc/2072-6651The 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.Kosuke TakadaKotone HamaTakaomi SasakiYuichi OtsukaMDPI AGarticlebacteriophage<i>Escherichia coli</i>toxin–antitoxin systemprophage inductionMedicineRENToxins, Vol 13, Iss 796, p 796 (2021)
institution DOAJ
collection DOAJ
language EN
topic bacteriophage
<i>Escherichia coli</i>
toxin–antitoxin system
prophage induction
Medicine
R
spellingShingle bacteriophage
<i>Escherichia coli</i>
toxin–antitoxin system
prophage induction
Medicine
R
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
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.
format article
author Kosuke Takada
Kotone Hama
Takaomi Sasaki
Yuichi Otsuka
author_facet Kosuke Takada
Kotone Hama
Takaomi Sasaki
Yuichi Otsuka
author_sort Kosuke Takada
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_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_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_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
publisher MDPI AG
publishDate 2021
url https://doaj.org/article/e17afaa5891843469b9e06e86380412c
work_keys_str_mv AT kosuketakada theihokwsokwilocusencodesatypeitoxinantitoxinsystemthatfacilitatesthereleaseoflysogenicsp5phageinenterohemorrhagiciescherichiacoliio157
AT kotonehama theihokwsokwilocusencodesatypeitoxinantitoxinsystemthatfacilitatesthereleaseoflysogenicsp5phageinenterohemorrhagiciescherichiacoliio157
AT takaomisasaki theihokwsokwilocusencodesatypeitoxinantitoxinsystemthatfacilitatesthereleaseoflysogenicsp5phageinenterohemorrhagiciescherichiacoliio157
AT yuichiotsuka theihokwsokwilocusencodesatypeitoxinantitoxinsystemthatfacilitatesthereleaseoflysogenicsp5phageinenterohemorrhagiciescherichiacoliio157
AT kosuketakada ihokwsokwilocusencodesatypeitoxinantitoxinsystemthatfacilitatesthereleaseoflysogenicsp5phageinenterohemorrhagiciescherichiacoliio157
AT kotonehama ihokwsokwilocusencodesatypeitoxinantitoxinsystemthatfacilitatesthereleaseoflysogenicsp5phageinenterohemorrhagiciescherichiacoliio157
AT takaomisasaki ihokwsokwilocusencodesatypeitoxinantitoxinsystemthatfacilitatesthereleaseoflysogenicsp5phageinenterohemorrhagiciescherichiacoliio157
AT yuichiotsuka ihokwsokwilocusencodesatypeitoxinantitoxinsystemthatfacilitatesthereleaseoflysogenicsp5phageinenterohemorrhagiciescherichiacoliio157
_version_ 1718410249571926016