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Uneven host cell growth causes lysogenic virus induction in the Baltic Sea

In the Baltic Sea redoxcline, lysogenic viruses infecting prokaryotes have rarely been detected using the commonly used inducing agent mitomycin C. However, it is well known that not all viruses are induceable by mitomycin C and growing evidence suggests that changes in trophic conditions may trigge...

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Autores principales: Köstner, Nicole, Jürgens, Klaus, Labrenz, Matthias, Herndl, Gerhard J., Winter, Christian
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6684075/
https://www.ncbi.nlm.nih.gov/pubmed/31386696
http://dx.doi.org/10.1371/journal.pone.0220716
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author Köstner, Nicole
Jürgens, Klaus
Labrenz, Matthias
Herndl, Gerhard J.
Winter, Christian
author_facet Köstner, Nicole
Jürgens, Klaus
Labrenz, Matthias
Herndl, Gerhard J.
Winter, Christian
author_sort Köstner, Nicole
collection PubMed
description In the Baltic Sea redoxcline, lysogenic viruses infecting prokaryotes have rarely been detected using the commonly used inducing agent mitomycin C. However, it is well known that not all viruses are induceable by mitomycin C and growing evidence suggests that changes in trophic conditions may trigger the induction of lysogenic viruses. We hypothesized that using antibiotics to simulate a strong change in trophic conditions for antibiotica-resistant cells due to reduced competition for resources might lead to the induction of lysogenic viruses into the lytic cycle within these cells. This hypothesis was tested by incubating prokaryotes obtained throughout the Baltic Sea redoxcline in seawater with substantially reduced numbers of viruses. We used a mixture of the protein synthesis-inhibiting antibiotics streptomycin and erythromycin to induce the desired changes in trophic conditions for resistant cells and at the same time ensuring that no progeny viruses were formed in sensitive cells. No inducible lysogenic viruses could be detected in incubations amended with mitomycin C. Yet, the presence of streptomycin and erythromycin increased virus-induced mortality of prokaryotes by 56–930% compared to controls, resulting in the induction of lysogenic viruses equivalent to 2–14% of in situ prokaryotic abundance. The results indicate the existence of a previously unrecognized induction mechanism for lysogenic viruses in the Baltic Sea redoxcline, as the mode of action distinctly differs between the used antibiotics (no virus production within affected cells) and mitomycin C (lysogenic viruses are produced within affected cells). Obtaining accurate experimental data on levels of lysogeny in prokaryotic host cells remains challenging, as relying on mitomycin C alone may severely underestimate lysogeny.
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spelling pubmed-66840752019-08-15 Uneven host cell growth causes lysogenic virus induction in the Baltic Sea Köstner, Nicole Jürgens, Klaus Labrenz, Matthias Herndl, Gerhard J. Winter, Christian PLoS One Research Article In the Baltic Sea redoxcline, lysogenic viruses infecting prokaryotes have rarely been detected using the commonly used inducing agent mitomycin C. However, it is well known that not all viruses are induceable by mitomycin C and growing evidence suggests that changes in trophic conditions may trigger the induction of lysogenic viruses. We hypothesized that using antibiotics to simulate a strong change in trophic conditions for antibiotica-resistant cells due to reduced competition for resources might lead to the induction of lysogenic viruses into the lytic cycle within these cells. This hypothesis was tested by incubating prokaryotes obtained throughout the Baltic Sea redoxcline in seawater with substantially reduced numbers of viruses. We used a mixture of the protein synthesis-inhibiting antibiotics streptomycin and erythromycin to induce the desired changes in trophic conditions for resistant cells and at the same time ensuring that no progeny viruses were formed in sensitive cells. No inducible lysogenic viruses could be detected in incubations amended with mitomycin C. Yet, the presence of streptomycin and erythromycin increased virus-induced mortality of prokaryotes by 56–930% compared to controls, resulting in the induction of lysogenic viruses equivalent to 2–14% of in situ prokaryotic abundance. The results indicate the existence of a previously unrecognized induction mechanism for lysogenic viruses in the Baltic Sea redoxcline, as the mode of action distinctly differs between the used antibiotics (no virus production within affected cells) and mitomycin C (lysogenic viruses are produced within affected cells). Obtaining accurate experimental data on levels of lysogeny in prokaryotic host cells remains challenging, as relying on mitomycin C alone may severely underestimate lysogeny. Public Library of Science 2019-08-06 /pmc/articles/PMC6684075/ /pubmed/31386696 http://dx.doi.org/10.1371/journal.pone.0220716 Text en © 2019 Köstner et al http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Article
Köstner, Nicole
Jürgens, Klaus
Labrenz, Matthias
Herndl, Gerhard J.
Winter, Christian
Uneven host cell growth causes lysogenic virus induction in the Baltic Sea
title Uneven host cell growth causes lysogenic virus induction in the Baltic Sea
title_full Uneven host cell growth causes lysogenic virus induction in the Baltic Sea
title_fullStr Uneven host cell growth causes lysogenic virus induction in the Baltic Sea
title_full_unstemmed Uneven host cell growth causes lysogenic virus induction in the Baltic Sea
title_short Uneven host cell growth causes lysogenic virus induction in the Baltic Sea
title_sort uneven host cell growth causes lysogenic virus induction in the baltic sea
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6684075/
https://www.ncbi.nlm.nih.gov/pubmed/31386696
http://dx.doi.org/10.1371/journal.pone.0220716
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