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Characterizing gene expression after expressing genetically encoded tools to change cellular NADH/NAD+ ratio in living cells

ABSTRACT: Characterizing gene expression after expressing genetically encoded tools to change cellular NADH/NAD+ ratio in living cells

PROVIDER: PRJNA970845 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24489331_1.fastq.gz	Fastqsanger.gz
	SRR24489331_2.fastq.gz	Fastqsanger.gz
	SRR24489332_1.fastq.gz	Fastqsanger.gz
	SRR24489332_2.fastq.gz	Fastqsanger.gz
	SRR24489333_1.fastq.gz	Fastqsanger.gz

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Characterizing gene expression after expressing genetically encoded tools to change cellular NADH/NAD+ ratio in living cells

Project description:To study the overabundance of reducing equivalents, termed reductive stress, specifically for NADH reductive stress, we introduce a soluble transhydrogenase from E. coli (EcSTH) as a novel genetically encoded tool to promote NADH overproduction

2023-09-01 | GSE232115 | GEO

Steroid Receptor Coactivator 1 is an Integrator of Glucose and NAD(+)/NADH Homeostasis

Project description:SRC-1 affects the expression of complex I of the mitochondrial electron transport chain, a set of enzymes responsible for the conversion of NADH to NAD(+). NAD(+) and NADH were subsequently identified as metabolites that underlie SRC-1's response to glucose deprivation. Knockdown of SRC-1 in glycolytic cancer cells abrogated their ability to grow in the absence of glucose consistent with SRC-1's role in promoting cellular adaptation to reduced glucose availability RNA profiling was used to examine the effects of SRC-1 perturbation on gene expression in the absence or presence of glucose.

2014-04-16 | E-GEOD-56843 | biostudies-arrayexpress

Steroid Receptor Coactivator 1 is an Integrator of Glucose and NAD(+)/NADH Homeostasis

2014-04-16 | GSE56843 | GEO

NAD+/NADH Redox Alterations Reconfigure Metabolism and Rejuvenate Senescent Human Mesenchymal Stem Cells In Vitro

Project description:Human mesenchymal stem cells (hMSCs) promote endogenous tissue regeneration and have become a promising candidate for cell therapy. However, in vitro culture expansion of hMSCs induces a rapid decline of stem cell properties through replicative senescence. Here we characterize metabolic profiles of hMSCs during expansion. We show that alterations of cellular nicotinamide adenine dinucleotide (NAD+ /NADH) redox balance and activity of the Sirtuin (Sirt) family enzymes regulate cellular senescence of hMSCs. Treatment with NAD+ precursor nicotinamide increases the intracellular NAD+ level and re-balances the NAD+ /NADH ratio, with enhanced Sirt-1 activity in hMSCs at high passage, partially restores mitochondrial fitness and rejuvenates senescent hMSCs. By contrast, human fibroblasts exhibit limited senescence as their cellular NAD+ /NADH balance is comparatively stable during expansion. These results indicate a potential metabolic and redox connection to replicative senescence in adult stem cells and identify NAD+ as a metabolic regulator that distinguishes stem cells from mature cells. This study also suggests potential strategies to maintain cellular homeostasis of hMSCs in clinical applications.

2021-09-09 | PXD022395 | Pride

Physiological responses of Saccharopolyspora erythraea towards perturbation of intracellular NADH/NAD+

Project description:Knowledge about effects of cofactor perturbation on cellular metabolism is scarce with respect to Saccharopolyspora erythraea. The water-forming NADH oxidase (NOX) from Streptococcus pneumonia was expressed in S.erythraea E3, an important industrial strain for erythromycin production, at three different levels to investigate effects of intracellular redox status on secondary metabolism. NOX expression reduced the intracellular [NADH]/[NAD+] ratios significantly, although with a strong constitutive promoter NOX function was limited due to the shortage of oxygen. We demonstrated the negative correlation between [NADH]/[NAD+] ratios and biosynthesis of erythromycin in S.erythraea, but a positive correlation between the redox ratios and pigment production as well. We furthermore completed next-generation RNA sequencing of E3 and two NOX-expression strains. The transcription results showed that transfer processes of carbohydrates, DNA and chemical groups were altered resulting in metabolic shifts to supply more NADH for NOX fully functioning. Additionally, redox status affected transcription of several genes by allosteric effects on their transcription initiation. Specifically, transcriptional analysis along with enzymatic assay suggested that redox status influenced biosynthesis of erythromycin indirectly by allosteric effects on biosynthesis of the secondary messenger, c-di-GMP. The present work provides a basis for future cofactor manipulation in S.erythraea for further improvement of erythromycin production.

2020-08-04 | GSE144067 | GEO

Physiological responses of Saccharopolyspora erythraea towards perturbation of intracellular NADH/NAD+

Project description:Physiological responses of Saccharopolyspora erythraea towards perturbation of intracellular NADH/NAD+

| PRJNA602682 | ENA

NADH Inhibition of SIRT1 Links Energy State to Transcription During Time-Restricted Feeding

Project description:In mammals, circadian rhythms are entrained to the light cycle and drive daily oscillations in levels of NAD+ a co-substrate of the class III histone deacetylase SIRT1 that associates with clock transcription factors. While NAD+ also participates in redox reactions, the extent to which NAD(H) couples nutrient state with circadian transcriptional cycles remains unknown. Here we show that nocturnal animals subjected to time-restricted feeding of a calorie-restricted diet (TRF-CR) only during nighttime display reduced body temperature and elevated hepatic NADH during daytime. Genetic uncoupling of nutrient state from NADH redox state through transduction of the water-forming NADH oxidase from Lactobacillus brevis (LbNOX) increases daytime body temperature and blood and liver acyl-carnitines. LbNOX expression in TRF-CR mice induces oxidative gene networks controlled by BMAL1 and PPARa and suppresses amino acid catabolic pathways. Enzymatic analyses reveal that NADH inhibits SIRT1 in vitro, corresponding with reduced deacetylation of SIRT1 substrates during TRF-CR in vivo. Remarkably, Sirt1 liver nullizygous animals subjected to TRF-CR display persistent hypothermia even when NADH is oxidized by LbNOX. Our findings reveal that the hepatic NADH cycle links nutrient state to whole-body energetics through the rhythmic regulation of SIRT1.

2021-10-08 | GSE151281 | GEO

Genetically encoded biosensors for evaluating NAD<sup>+</sup>/NADH ratio in cytosolic and mitochondrial compartments.

Project description:The ratio of oxidized to reduced NAD (NAD+/NADH) sets intracellular redox balance and antioxidant capacity. Intracellular NAD is compartmentalized and the mitochondrial NAD+/NADH ratio is intricately linked to cellular function. Here, we report the monitoring of the NAD+/NADH ratio in mitochondrial and cytosolic compartments in live cells by using a modified genetic biosensor (SoNar). The fluorescence signal of SoNar targeted to mitochondria (mt-SoNar) or cytosol (ct-SoNar) responded linearly to physiological NAD+/NADH ratios in situ. NAD+/NADH ratios in cytosol versus mitochondria responded rapidly, but differently, to acute metabolic perturbations, indicating distinct NAD pools. Subcellular NAD redox balance regained homeostasis via communications through malate-aspartate shuttle. Mitochondrial and cytosolic NAD+/NADH ratios are influenced by NAD+ precursor levels and are distinctly regulated under pathophysiological conditions. Compartment-targeted biosensors and real-time imaging allow assessment of subcellular NAD+/NADH redox signaling in live cells, enabling future mechanistic research of NAD redox in cell biology and disease development.

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The Malate Shuttle Detoxifies Ammonia in Exhausted T Cells by Producing 2-Ketoglutarate

Project description:The malate shuttle is traditionally known to maintain the NAD+/NADH balance between the cytosol and mitochondria. Whether the malate shuttle has additional functions was unknown. Here we show that chronic viral infections induced the expression of GOT1, the key enzyme in the malate shuttle, in CD8+ T cells. Got1 deficiency indeed decreased the NAD+/NADH ratio and dampened antiviral CD8+ T cell responses to chronic infection; however, increasing the NAD+/NADH ratio did not restore antiviral T cell responses. Got1 deficiency reduced the production of the ammonia scavenger 2-ketoglutarate and led to toxic ammonia accumulation in CD8+ T cells. Supplementation with 2-ketoglutarate assimilated and detoxified ammonia in Got1-deficient T cells and restored antiviral responses. This study suggests that the major function of the malate shuttle in CD8+ T cells is not to maintain the NAD+/NADH ratio, but rather to detoxify ammonia and enable sustainable ammonia-neutral glutamine catabolism in CD8+ T cells during chronic infections.

2023-09-01 | GSE220876 | GEO

Gene expression profile of SoNar-high and SoNar-low B-cell acute lymphoblastic leukemia (B-ALL) cells

Project description:To dissect the metabolic state of B-ALL cells, we have developed a genetically encoded fluorescent sensor (SoNar) for tracking cytosolic NADH and NAD+ redox states and constructed the transgenic mouse. Based on the NADH/NAD+ ratio, we have sorted SoNar-high and SoNar-low B-ALL cells to employ whole genome microarray expression profiling as a discovery platform to identify genes with the potential to regulate the metabolism of B-ALL cells.

2018-02-06 | GSE110111 | GEO

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