Suitable extracellular oxidoreduction potential inhibit rex regulation and effect central carbon and energy metabolism in Saccharopolyspora spinosa

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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KSHV Reprogramming of Host Energy Metabolism for Pathogenesis

Frontiers in Cellular and Infection Microbiology ◽

10.3389/fcimb.2021.621156 ◽

2021 ◽

Vol 11 ◽

Author(s):

Xiaoqing Liu ◽

Caixia Zhu ◽

Yuyan Wang ◽

Fang Wei ◽

Qiliang Cai

Keyword(s):

Energy Metabolism ◽

Metabolic Pathways ◽

B Lymphocyte ◽

Aerobic Glycolysis ◽

Cell Metabolism ◽

Acid Synthesis ◽

Central Carbon Metabolism ◽

Central Carbon ◽

Cell Energy ◽

Infected Cells

Reprogramming of energy metabolism is a key for cancer development. Kaposi’s sarcoma-associated herpesvirus (KSHV), a human oncogenic herpesvirus, is tightly associated with several human malignancies by infecting B-lymphocyte or endothelial cells. Cancer cell energy metabolism is mainly dominated by three pathways of central carbon metabolism, including aerobic glycolysis, glutaminolysis, and fatty acid synthesis. Increasing evidence has shown that KSHV infection can alter central carbon metabolic pathways to produce biomass for viral replication, as well as the survival and proliferation of infected cells. In this review, we summarize recent studies exploring how KSHV manipulates host cell metabolism to promote viral pathogenesis, which provides the potential therapeutic targets and strategies for KSHV-associated cancers.

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Metabolomics analysis reveals that myrcene stimulates the spore germination of Penicillium digitatum via the upregulation of central carbon and energy metabolism

Postharvest Biology and Technology ◽

10.1016/j.postharvbio.2020.111329 ◽

2020 ◽

Vol 170 ◽

pp. 111329 ◽

Cited By ~ 1

Author(s):

Jinxin Che ◽

Yue Chen ◽

Yalan Wu ◽

Lu Li ◽

Nengguo Tao

Keyword(s):

Energy Metabolism ◽

Spore Germination ◽

Penicillium Digitatum ◽

Central Carbon ◽

Metabolomics Analysis

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CceR and AkgR Regulate Central Carbon and Energy Metabolism in Alphaproteobacteria

mBio ◽

10.1128/mbio.02461-14 ◽

2015 ◽

Vol 6 (1) ◽

Cited By ~ 9

Author(s):

Saheed Imam ◽

Daniel R. Noguera ◽

Timothy J. Donohue

Keyword(s):

Energy Metabolism ◽

Central Carbon

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The RNA-binding protein RBP42 regulates cellular energy metabolism in mammalian-infective Trypanosoma brucei

10.1101/2021.04.14.439849 ◽

2021 ◽

Author(s):

Anish Das ◽

Tong Liu ◽

Hong Li ◽

Seema Husain

Keyword(s):

Energy Metabolism ◽

Rna Binding ◽

Binding Protein ◽

Critical Role ◽

Rna Binding Protein ◽

Mrna Translation ◽

Cellular Energy ◽

Target Mrna ◽

Cellular Energy Metabolism ◽

Central Carbon

AbstractRNA-binding proteins are key players in coordinated post-transcriptional regulation of functionally related genes, defined as RNA regulons. RNA regulons play particularly critical roles in parasitic trypanosomes, which exhibit unregulated co-transcription of long arrays of unrelated genes. In this report, we present a systematic analysis of an essential RNA-binding protein, RBP42, in the mammalian-infective slender bloodstream form of African trypanosome, and we show that RBP42 is a key regulator of parasite’s central carbon and energy metabolism. Using individual-nucleotide resolution UV cross-linking and immunoprecipitation (iCLIP) to identify genome-wide RBP42-RNA interactions, we show that RBP42 preferentially binds within the coding region of mRNAs encoding core metabolic enzymes. Using global quantitative transcriptomic and proteomic analyses, we also show that loss of RBP42 reduces the abundance of target mRNA-encoded proteins, but not target mRNA, suggesting a plausible role of RBP42 as a positive regulator of target mRNA translation. Analysis reveals significant changes in central carbon metabolic intermediates following loss of RBP42, further supporting its critical role in cellular energy metabolism.

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The Central Carbon and Energy Metabolism of Marine Diatoms

Metabolites ◽

10.3390/metabo3020325 ◽

2013 ◽

Vol 3 (2) ◽

pp. 325-346 ◽

Cited By ~ 38

Author(s):

Toshihiro Obata ◽

Alisdair Fernie ◽

Adriano Nunes-Nesi

Keyword(s):

Energy Metabolism ◽

Marine Diatoms ◽

Central Carbon

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Involvement of mitochondria in the control of plant cell NAD(P)H reduction levels

Biochemical Society Transactions ◽

10.1042/bst0380661 ◽

2010 ◽

Vol 38 (2) ◽

pp. 661-666 ◽

Cited By ~ 24

Author(s):

Allan G. Rasmusson ◽

Sabá V. Wallström

Keyword(s):

Energy Metabolism ◽

Metabolic Pathways ◽

Pentose Phosphate ◽

Cellular Processes ◽

Functional Interactions ◽

Central Carbon ◽

Important Regulator ◽

Nadph Oxidation ◽

Set Up ◽

Stress Dependent

NADPH and NADH mediate reductant flow between cellular processes, linking central carbon and energy metabolism with intermediary metabolism, stress defence and development. Recent investigations have revealed paths of functional interactions, and have suggested that mitochondrial NADPH oxidation, especially together with the oxidative pentose phosphate pathway, is an important regulator of the cytosolic NADPH reduction level. Furthermore, stress-dependent metabolic pathways substantially affect the NADPH reduction level in particular physiological situations. The mitochondrial impact on the NADPH reduction level provides a model example of the physiological significance of the mitochondrial NAD(P)H dehydrogenase set-up, which is more complex in plants than in other organisms.

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