PknG senses amino acid availability to control metabolism and virulence of Mycobacterium tuberculosis
Fig 7
Deletion of garA or disruption of GarA phosphorylation caused changes in intracellular glutamate and other changes in the metabolome of M. smegmatis.
Intracellular metabolites from wild type M. smegmatis and mutants were analysed by mass spectrometry using an untargeted metabolomics approach. M. smegmatis lacking garA has lower intracellular glutamate and metabolites related to glutamate than the parental strain (A) but plasmid encoded GarA reversed this change (B). M. smegmatis expressing truncated GarA that lacks phosphorylation sites had higher intracellular ornithine than wild type (C). Intracellular glutamate concentrations for the mutant strains are compared to wild type in panel (D), together with those metabolites that were significantly changed in >1 mutant strain but not in complemented strains. pSer is O-phosphoserine, Orn is ornithine, Cit is citrulline, MaltoP is maltopentaose. (A-C) Each point on the scatter plots represents a single metabolite. Metabolites with the greatest fold-change and statistical significance are highlighted (log2(fold change)>0.5 and q-value<0.05), thresholds marked as dashed lines on graphs): metabolites at lower concentration are blue and those at higher concentration are red. These data were taken from cells growing in Middlebrook 7H9 in early exponential phase and represent the mean from at least 3 independent experiments.