Abstract
Arsenite (AsIII) oxidation is a microbially-catalyzed transformation that directly impacts arsenic toxicity, bioaccumulation, and bioavailability in environmental systems. The genes for AsIII oxidation (aio) encode a periplasmic AsIII sensor AioX, transmembrane histidine kinase AioS, and cognate regulatory partner AioR, which control expression of the AsIII oxidase AioBA. The aio genes are under ultimate control of the phosphate stress response via histidine kinase PhoR. To better understand the cell-wide impacts exerted by these key histidine kinases, we employed 1H nuclear magnetic resonance (1H NMR) and liquid chromatography-coupled mass spectrometry (LC-MS) metabolomics to characterize the metabolic profiles of ΔphoR and ΔaioS mutants of Agrobacterium tumefaciens 5A during AsIII oxidation. The data reveals a smaller group of metabolites impacted by the ΔaioS mutation, including hypoxanthine and various maltose derivatives, while a larger impact is observed for the ΔphoR mutation, influencing betaine, glutamate, and different sugars. The metabolomics data were integrated with previously published transcriptomics analyses to detail pathways perturbed during AsIII oxidation and those modulated by PhoR and/or AioS. The results highlight considerable disruptions in central carbon metabolism in the ΔphoR mutant. These data provide a detailed map of the metabolic impacts of AsIII, PhoR, and/or AioS, and inform current paradigms concerning arsenic–microbe interactions and nutrient cycling in contaminated environments.
Highlights
Arsenic is the highest priority EPA contaminant due to its prevalence, toxicity, and potential for wide-spread human exposure [1]
The present study focused on parallel analyses of metabolic changes occurring in ∆phoR and ∆aioS mutant strains, utilizing 1H nuclear magnetic resonance (1H nuclear magnetic resonance (NMR)) and liquid chromatography-coupled mass spectrometry (LC-MS) for untargeted metabolomics analysis
Research on arsenic contamination.Arsenite (AsIII)-resistant organisms has characterized various functions induced by AsIII exposure [11,29,30,31,32,33], ranging from direct arsenic responses like arsenic resistance, AsIII oxidation and oxidative stress, to general cell functions including remodeling of carbon and amino acid metabolic pathways
Summary
Arsenic is the highest priority EPA contaminant due to its prevalence, toxicity, and potential for wide-spread human exposure [1]. The AsIII oxidase (AioBA) is regulated by a three-component signal transduction system: periplasmic AsIII sensor protein (AioX), histidine kinase (AioS), and its cognate regulatory partner (AioR) [5,6]. The PSR is regulated through a two-component signal transduction system (PhoR/PhoB), where the histidine kinase PhoR is the master regulator controlling expression of aioSRBA [8], in addition to the well-defined PSR genes [9,10]. Cross talk between these two regulatory pairs, PhoR/PhoB and AioS/AioR, has been demonstrated [8]. Improved growth under low-Pi conditions following AsIII exposure and evidence for partial incorporation of AsV into cellular lipids in A. tumefaciens 5A [8] indicate a close relationship between these regulatory components
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