PknG senses amino acid availability to control metabolism and virulence of Mycobacterium tuberculosis.

Sensing and response to changes in nutrient availability are essential for the lifestyle of environmental and pathogenic bacteria. Serine/threonine protein kinase G (PknG) is required for virulence of the human pathogen Mycobacterium tuberculosis, and its putative substrate GarA regulates the tricar...

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Main Authors: Barbara Rieck, Giulia Degiacomi, Michael Zimmermann, Alessandro Cascioferro, Francesca Boldrin, Natalie R Lazar-Adler, Andrew R Bottrill, Fabien le Chevalier, Wafa Frigui, Marco Bellinzoni, María-Natalia Lisa, Pedro M Alzari, Liem Nguyen, Roland Brosch, Uwe Sauer, Riccardo Manganelli, Helen M O'Hare
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2017-05-01
Series:PLoS Pathogens
Online Access:https://journals.plos.org/plospathogens/article/file?id=10.1371/journal.ppat.1006399&type=printable
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author Barbara Rieck
Giulia Degiacomi
Michael Zimmermann
Alessandro Cascioferro
Francesca Boldrin
Natalie R Lazar-Adler
Andrew R Bottrill
Fabien le Chevalier
Wafa Frigui
Marco Bellinzoni
María-Natalia Lisa
Pedro M Alzari
Liem Nguyen
Roland Brosch
Uwe Sauer
Riccardo Manganelli
Helen M O'Hare
author_facet Barbara Rieck
Giulia Degiacomi
Michael Zimmermann
Alessandro Cascioferro
Francesca Boldrin
Natalie R Lazar-Adler
Andrew R Bottrill
Fabien le Chevalier
Wafa Frigui
Marco Bellinzoni
María-Natalia Lisa
Pedro M Alzari
Liem Nguyen
Roland Brosch
Uwe Sauer
Riccardo Manganelli
Helen M O'Hare
author_sort Barbara Rieck
collection DOAJ
description Sensing and response to changes in nutrient availability are essential for the lifestyle of environmental and pathogenic bacteria. Serine/threonine protein kinase G (PknG) is required for virulence of the human pathogen Mycobacterium tuberculosis, and its putative substrate GarA regulates the tricarboxylic acid cycle in M. tuberculosis and other Actinobacteria by protein-protein binding. We sought to understand the stimuli that lead to phosphorylation of GarA, and the roles of this regulatory system in pathogenic and non-pathogenic bacteria. We discovered that M. tuberculosis lacking garA was severely attenuated in mice and macrophages and furthermore that GarA lacking phosphorylation sites failed to restore the growth of garA deficient M. tuberculosis in macrophages. Additionally we examined the impact of genetic disruption of pknG or garA upon protein phosphorylation, nutrient utilization and the intracellular metabolome. We found that phosphorylation of GarA requires PknG and depends on nutrient availability, with glutamate and aspartate being the main stimuli. Disruption of pknG or garA caused opposing effects on metabolism: a defect in glutamate catabolism or depletion of intracellular glutamate, respectively. Strikingly, disruption of the phosphorylation sites of GarA was sufficient to recapitulate defects caused by pknG deletion. The results suggest that GarA is a cellular target of PknG and the metabolomics data demonstrate that the function of this signaling system is in metabolic regulation. This function in amino acid homeostasis is conserved amongst the Actinobacteria and provides an example of the close relationship between metabolism and virulence.
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spelling doaj-art-fcfce8ed562f48a58fcab50a5ba17c922025-08-20T03:24:27ZengPublic Library of Science (PLoS)PLoS Pathogens1553-73661553-73742017-05-01135e100639910.1371/journal.ppat.1006399PknG senses amino acid availability to control metabolism and virulence of Mycobacterium tuberculosis.Barbara RieckGiulia DegiacomiMichael ZimmermannAlessandro CascioferroFrancesca BoldrinNatalie R Lazar-AdlerAndrew R BottrillFabien le ChevalierWafa FriguiMarco BellinzoniMaría-Natalia LisaPedro M AlzariLiem NguyenRoland BroschUwe SauerRiccardo ManganelliHelen M O'HareSensing and response to changes in nutrient availability are essential for the lifestyle of environmental and pathogenic bacteria. Serine/threonine protein kinase G (PknG) is required for virulence of the human pathogen Mycobacterium tuberculosis, and its putative substrate GarA regulates the tricarboxylic acid cycle in M. tuberculosis and other Actinobacteria by protein-protein binding. We sought to understand the stimuli that lead to phosphorylation of GarA, and the roles of this regulatory system in pathogenic and non-pathogenic bacteria. We discovered that M. tuberculosis lacking garA was severely attenuated in mice and macrophages and furthermore that GarA lacking phosphorylation sites failed to restore the growth of garA deficient M. tuberculosis in macrophages. Additionally we examined the impact of genetic disruption of pknG or garA upon protein phosphorylation, nutrient utilization and the intracellular metabolome. We found that phosphorylation of GarA requires PknG and depends on nutrient availability, with glutamate and aspartate being the main stimuli. Disruption of pknG or garA caused opposing effects on metabolism: a defect in glutamate catabolism or depletion of intracellular glutamate, respectively. Strikingly, disruption of the phosphorylation sites of GarA was sufficient to recapitulate defects caused by pknG deletion. The results suggest that GarA is a cellular target of PknG and the metabolomics data demonstrate that the function of this signaling system is in metabolic regulation. This function in amino acid homeostasis is conserved amongst the Actinobacteria and provides an example of the close relationship between metabolism and virulence.https://journals.plos.org/plospathogens/article/file?id=10.1371/journal.ppat.1006399&type=printable
spellingShingle Barbara Rieck
Giulia Degiacomi
Michael Zimmermann
Alessandro Cascioferro
Francesca Boldrin
Natalie R Lazar-Adler
Andrew R Bottrill
Fabien le Chevalier
Wafa Frigui
Marco Bellinzoni
María-Natalia Lisa
Pedro M Alzari
Liem Nguyen
Roland Brosch
Uwe Sauer
Riccardo Manganelli
Helen M O'Hare
PknG senses amino acid availability to control metabolism and virulence of Mycobacterium tuberculosis.
PLoS Pathogens
title PknG senses amino acid availability to control metabolism and virulence of Mycobacterium tuberculosis.
title_full PknG senses amino acid availability to control metabolism and virulence of Mycobacterium tuberculosis.
title_fullStr PknG senses amino acid availability to control metabolism and virulence of Mycobacterium tuberculosis.
title_full_unstemmed PknG senses amino acid availability to control metabolism and virulence of Mycobacterium tuberculosis.
title_short PknG senses amino acid availability to control metabolism and virulence of Mycobacterium tuberculosis.
title_sort pkng senses amino acid availability to control metabolism and virulence of mycobacterium tuberculosis
url https://journals.plos.org/plospathogens/article/file?id=10.1371/journal.ppat.1006399&type=printable
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