scholarly journals Metabolic Responses to Arsenite Exposure Regulated through Histidine Kinases PhoR and AioS in Agrobacterium tumefaciens 5A

2020 ◽  
Vol 8 (9) ◽  
pp. 1339
Author(s):  
Rachel A. Rawle ◽  
Monika Tokmina-Lukaszewska ◽  
Zunji Shi ◽  
Yoon-Suk Kang ◽  
Brian P. Tripet ◽  
...  
Keyword(s):  
Agrobacterium Tumefaciens ◽  
Histidine Kinase ◽  
Central Carbon Metabolism ◽  
Arsenic Toxicity ◽  
Histidine Kinases ◽  
Metabolomics Data ◽  
1H Nuclear Magnetic Resonance ◽  
Central Carbon ◽  
Microbe Interactions ◽  
Ultimate Control

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.

scholarly journals Metformin Targets Central Carbon Metabolism and Reveals Mitochondrial Requirements in Human Cancers

2016 ◽  
Vol 24 (5) ◽  
pp. 728-739 ◽  
Author(s):  
Xiaojing Liu ◽  
Iris L. Romero ◽  
Lacey M. Litchfield ◽  
Ernst Lengyel ◽  
Jason W. Locasale
Keyword(s):  
Carbon Metabolism ◽  
Central Carbon Metabolism ◽  
Human Cancers ◽  
Central Carbon

Trisomy 21 results in modest impacts on mitochondrial function and central carbon metabolism

2021 ◽  
Author(s):  
Colin C. Anderson ◽  
John O. Marentette ◽  
Kendra M. Prutton ◽  
Abhishek K. Rauniyar ◽  
Julie A. Reisz ◽  
...  
Keyword(s):  
Mitochondrial Function ◽  
Carbon Metabolism ◽  
Trisomy 21 ◽  
Central Carbon Metabolism ◽  
Central Carbon

Metabolic phenotyping of the Yersinia high-pathogenicity island that regulates central carbon metabolism

The Analyst ◽  
2015 ◽  
Vol 140 (10) ◽  
pp. 3356-3361 ◽  
Author(s):  
Leyu Yan ◽  
Wenna Nie ◽  
Haitao Lv
Keyword(s):  
Carbon Metabolism ◽  
Virulence Genes ◽  
Pathogenicity Island ◽  
Central Carbon Metabolism ◽  
Metabolic Phenotyping ◽  
High Pathogenicity ◽  
Central Carbon ◽  
Regulatory Effects

The regulatory effects of the HPI virulence genes on central carbon metabolism differentiate UPEC from non-UPEC.

scholarly journals HexR Controls Glucose-Responsive Genes and Central Carbon Metabolism in Neisseria meningitidis

2015 ◽  
Vol 198 (4) ◽  
pp. 644-654 ◽  
Author(s):  
Ana Antunes ◽  
Giacomo Golfieri ◽  
Francesca Ferlicca ◽  
Marzia M. Giuliani ◽  
Vincenzo Scarlato ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Neisseria Meningitidis ◽  
Microarray Analysis ◽  
Carbon Metabolism ◽  
Tricarboxylic Acid Cycle ◽  
Transcriptional Regulator ◽  
Central Carbon Metabolism ◽  
Binding Motif ◽  
Content Type ◽  
Central Carbon

ABSTRACTNeisseria meningitidis, an exclusively human pathogen and the leading cause of bacterial meningitis, must adapt to different host niches during human infection.N. meningitidiscan utilize a restricted range of carbon sources, including lactate, glucose, and pyruvate, whose concentrations vary in host niches. Microarray analysis ofN. meningitidisgrown in a chemically defined medium in the presence or absence of glucose allowed us to identify genes regulated by carbon source availability. Most such genes are implicated in energy metabolism and transport, and some are implicated in virulence. In particular, genes involved in glucose catabolism were upregulated, whereas genes involved in the tricarboxylic acid cycle were downregulated. Several genes encoding surface-exposed proteins, including the MafA adhesins andNeisseriasurface protein A, were upregulated in the presence of glucose. Our microarray analysis led to the identification of a glucose-responsivehexR-like transcriptional regulator that controls genes of the central carbon metabolism ofN. meningitidisin response to glucose. We characterized the HexR regulon and showed that thehexRgene is accountable for some of the glucose-responsive regulation;in vitroassays with the purified protein showed that HexR binds to the promoters of the central metabolic operons of the bacterium. Based on DNA sequence alignment of the target sites, we propose a 17-bp pseudopalindromic consensus HexR binding motif. Furthermore,N. meningitidisstrains lackinghexRexpression were deficient in establishing successful bacteremia in an infant rat model of infection, indicating the importance of this regulator for the survival of this pathogenin vivo.IMPORTANCENeisseria meningitidisgrows on a limited range of nutrients during infection. We analyzed the gene expression ofN. meningitidisin response to glucose, the main energy source available in human blood, and we found that glucose regulates many genes implicated in energy metabolism and nutrient transport, as well as some implicated in virulence. We identified and characterized a transcriptional regulator (HexR) that controls metabolic genes ofN. meningitidisin response to glucose. We generated a mutant lacking HexR and found that the mutant was impaired in causing systemic infection in animal models. SinceN. meningitidislacks known bacterial regulators of energy metabolism, our findings suggest that HexR plays a major role in its biology by regulating metabolism in response to environmental signals.

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