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Interactions between the Prophage 919TP and Its Vibrio cholerae Host: Implications of gmd Mutation for Phage Resistance, Cell Auto-Aggregation, and Motility

Prophage 919TP is widely distributed among Vibrio cholera and is induced to produce free φ919TP phage particles. However, the interactions between prophage φ919TP, the induced phage particle, and its host remain unknown. In particular, phage resistance mechanisms and potential fitness trade-offs, re...

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Autores principales: Li, Na, Zeng, Yigang, Hu, Bijie, Zhu, Tongyu, Svenningsen, Sine Lo, Middelboe, Mathias, Tan, Demeng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8706939/
https://www.ncbi.nlm.nih.gov/pubmed/34960610
http://dx.doi.org/10.3390/v13122342
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author Li, Na
Zeng, Yigang
Hu, Bijie
Zhu, Tongyu
Svenningsen, Sine Lo
Middelboe, Mathias
Tan, Demeng
author_facet Li, Na
Zeng, Yigang
Hu, Bijie
Zhu, Tongyu
Svenningsen, Sine Lo
Middelboe, Mathias
Tan, Demeng
author_sort Li, Na
collection PubMed
description Prophage 919TP is widely distributed among Vibrio cholera and is induced to produce free φ919TP phage particles. However, the interactions between prophage φ919TP, the induced phage particle, and its host remain unknown. In particular, phage resistance mechanisms and potential fitness trade-offs, resulting from phage resistance, are unresolved. In this study, we examined a prophage 919TP-deleted variant of V. cholerae and its interaction with a modified lytic variant of the induced prophage (φ919TP cI(-)). Specifically, the phage-resistant mutant was isolated by challenging a prophage-deleted variant with lytic phage φ919TP cI(-). Further, the comparative genomic analysis of wild-type and φ919TP cI(-)-resistant mutant predicted that phage φ919TP cI(-) selects for phage-resistant mutants harboring a mutation in key steps of lipopolysaccharide (LPS) O-antigen biosynthesis, causing a single-base-pair deletion in gene gmd. Our study showed that the gmd-mediated O-antigen defect can cause pleiotropic phenotypes, e.g., cell autoaggregation and reduced swarming motility, emphasizing the role of phage-driven diversification in V. cholerae. The developed approach assists in the identification of genetic determinants of host specificity and is used to explore the molecular mechanism underlying phage-host interactions. Our findings contribute to the understanding of prophage-facilitated horizontal gene transfer and emphasize the potential for developing new strategies to optimize the use of phages in bacterial pathogen control.
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spelling pubmed-87069392021-12-25 Interactions between the Prophage 919TP and Its Vibrio cholerae Host: Implications of gmd Mutation for Phage Resistance, Cell Auto-Aggregation, and Motility Li, Na Zeng, Yigang Hu, Bijie Zhu, Tongyu Svenningsen, Sine Lo Middelboe, Mathias Tan, Demeng Viruses Article Prophage 919TP is widely distributed among Vibrio cholera and is induced to produce free φ919TP phage particles. However, the interactions between prophage φ919TP, the induced phage particle, and its host remain unknown. In particular, phage resistance mechanisms and potential fitness trade-offs, resulting from phage resistance, are unresolved. In this study, we examined a prophage 919TP-deleted variant of V. cholerae and its interaction with a modified lytic variant of the induced prophage (φ919TP cI(-)). Specifically, the phage-resistant mutant was isolated by challenging a prophage-deleted variant with lytic phage φ919TP cI(-). Further, the comparative genomic analysis of wild-type and φ919TP cI(-)-resistant mutant predicted that phage φ919TP cI(-) selects for phage-resistant mutants harboring a mutation in key steps of lipopolysaccharide (LPS) O-antigen biosynthesis, causing a single-base-pair deletion in gene gmd. Our study showed that the gmd-mediated O-antigen defect can cause pleiotropic phenotypes, e.g., cell autoaggregation and reduced swarming motility, emphasizing the role of phage-driven diversification in V. cholerae. The developed approach assists in the identification of genetic determinants of host specificity and is used to explore the molecular mechanism underlying phage-host interactions. Our findings contribute to the understanding of prophage-facilitated horizontal gene transfer and emphasize the potential for developing new strategies to optimize the use of phages in bacterial pathogen control. MDPI 2021-11-23 /pmc/articles/PMC8706939/ /pubmed/34960610 http://dx.doi.org/10.3390/v13122342 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Li, Na
Zeng, Yigang
Hu, Bijie
Zhu, Tongyu
Svenningsen, Sine Lo
Middelboe, Mathias
Tan, Demeng
Interactions between the Prophage 919TP and Its Vibrio cholerae Host: Implications of gmd Mutation for Phage Resistance, Cell Auto-Aggregation, and Motility
title Interactions between the Prophage 919TP and Its Vibrio cholerae Host: Implications of gmd Mutation for Phage Resistance, Cell Auto-Aggregation, and Motility
title_full Interactions between the Prophage 919TP and Its Vibrio cholerae Host: Implications of gmd Mutation for Phage Resistance, Cell Auto-Aggregation, and Motility
title_fullStr Interactions between the Prophage 919TP and Its Vibrio cholerae Host: Implications of gmd Mutation for Phage Resistance, Cell Auto-Aggregation, and Motility
title_full_unstemmed Interactions between the Prophage 919TP and Its Vibrio cholerae Host: Implications of gmd Mutation for Phage Resistance, Cell Auto-Aggregation, and Motility
title_short Interactions between the Prophage 919TP and Its Vibrio cholerae Host: Implications of gmd Mutation for Phage Resistance, Cell Auto-Aggregation, and Motility
title_sort interactions between the prophage 919tp and its vibrio cholerae host: implications of gmd mutation for phage resistance, cell auto-aggregation, and motility
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8706939/
https://www.ncbi.nlm.nih.gov/pubmed/34960610
http://dx.doi.org/10.3390/v13122342
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