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Revisiting the role of phospholipases C in virulence and the lifecycle of Mycobacterium tuberculosis

Mycobacterium tuberculosis, the agent of human tuberculosis has developed different virulence mechanisms and virulence-associated tools during its evolution to survive and multiply inside the host. Based on previous reports and by analogy with other bacteria, phospholipases C (PLC) of M. tuberculosi...

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Autores principales: Le Chevalier, Fabien, Cascioferro, Alessandro, Frigui, Wafa, Pawlik, Alexandre, Boritsch, Eva C., Bottai, Daria, Majlessi, Laleh, Herrmann, Jean Louis, Brosch, Roland
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4658479/
https://www.ncbi.nlm.nih.gov/pubmed/26603639
http://dx.doi.org/10.1038/srep16918
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author Le Chevalier, Fabien
Cascioferro, Alessandro
Frigui, Wafa
Pawlik, Alexandre
Boritsch, Eva C.
Bottai, Daria
Majlessi, Laleh
Herrmann, Jean Louis
Brosch, Roland
author_facet Le Chevalier, Fabien
Cascioferro, Alessandro
Frigui, Wafa
Pawlik, Alexandre
Boritsch, Eva C.
Bottai, Daria
Majlessi, Laleh
Herrmann, Jean Louis
Brosch, Roland
author_sort Le Chevalier, Fabien
collection PubMed
description Mycobacterium tuberculosis, the agent of human tuberculosis has developed different virulence mechanisms and virulence-associated tools during its evolution to survive and multiply inside the host. Based on previous reports and by analogy with other bacteria, phospholipases C (PLC) of M. tuberculosis were thought to be among these tools. To get deeper insights into the function of PLCs, we investigated their putative involvement in the intracellular lifestyle of M. tuberculosis, with emphasis on phagosomal rupture and virulence, thereby re-visiting a research theme of longstanding interest. Through the construction and use of an M. tuberculosis H37Rv PLC-null mutant (ΔPLC) and control strains, we found that PLCs of M. tuberculosis were not required for induction of phagosomal rupture and only showed marginal, if any, impact on virulence of M. tuberculosis in the cellular and mouse infection models used in this study. In contrast, we found that PLC-encoding genes were strongly upregulated under phosphate starvation and that PLC-proficient M. tuberculosis strains survived better than ΔPLC mutants under conditions where phosphatidylcholine served as sole phosphate source, opening new perspectives for studies on the role of PLCs in the lifecycle of M. tuberculosis.
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spelling pubmed-46584792015-11-30 Revisiting the role of phospholipases C in virulence and the lifecycle of Mycobacterium tuberculosis Le Chevalier, Fabien Cascioferro, Alessandro Frigui, Wafa Pawlik, Alexandre Boritsch, Eva C. Bottai, Daria Majlessi, Laleh Herrmann, Jean Louis Brosch, Roland Sci Rep Article Mycobacterium tuberculosis, the agent of human tuberculosis has developed different virulence mechanisms and virulence-associated tools during its evolution to survive and multiply inside the host. Based on previous reports and by analogy with other bacteria, phospholipases C (PLC) of M. tuberculosis were thought to be among these tools. To get deeper insights into the function of PLCs, we investigated their putative involvement in the intracellular lifestyle of M. tuberculosis, with emphasis on phagosomal rupture and virulence, thereby re-visiting a research theme of longstanding interest. Through the construction and use of an M. tuberculosis H37Rv PLC-null mutant (ΔPLC) and control strains, we found that PLCs of M. tuberculosis were not required for induction of phagosomal rupture and only showed marginal, if any, impact on virulence of M. tuberculosis in the cellular and mouse infection models used in this study. In contrast, we found that PLC-encoding genes were strongly upregulated under phosphate starvation and that PLC-proficient M. tuberculosis strains survived better than ΔPLC mutants under conditions where phosphatidylcholine served as sole phosphate source, opening new perspectives for studies on the role of PLCs in the lifecycle of M. tuberculosis. Nature Publishing Group 2015-11-25 /pmc/articles/PMC4658479/ /pubmed/26603639 http://dx.doi.org/10.1038/srep16918 Text en Copyright © 2015, Macmillan Publishers Limited http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
spellingShingle Article
Le Chevalier, Fabien
Cascioferro, Alessandro
Frigui, Wafa
Pawlik, Alexandre
Boritsch, Eva C.
Bottai, Daria
Majlessi, Laleh
Herrmann, Jean Louis
Brosch, Roland
Revisiting the role of phospholipases C in virulence and the lifecycle of Mycobacterium tuberculosis
title Revisiting the role of phospholipases C in virulence and the lifecycle of Mycobacterium tuberculosis
title_full Revisiting the role of phospholipases C in virulence and the lifecycle of Mycobacterium tuberculosis
title_fullStr Revisiting the role of phospholipases C in virulence and the lifecycle of Mycobacterium tuberculosis
title_full_unstemmed Revisiting the role of phospholipases C in virulence and the lifecycle of Mycobacterium tuberculosis
title_short Revisiting the role of phospholipases C in virulence and the lifecycle of Mycobacterium tuberculosis
title_sort revisiting the role of phospholipases c in virulence and the lifecycle of mycobacterium tuberculosis
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4658479/
https://www.ncbi.nlm.nih.gov/pubmed/26603639
http://dx.doi.org/10.1038/srep16918
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