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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression profiling of attenuated mitochondrial function identifies retrograde signals in Drosophila

ABSTRACT: Mitochondria are able to modulate cell state and fate during normal and pathophysiologic conditions through a nuclear mediated mechanism collectively termed as a retrograde response. Our previous studies in Drosophila have clearly established that progress through the cell cycle is precisely regulated by the intrinsic activity of the mitochondrion by specific signaling cascades mounted by the cell. As a means to further our understanding of how mitochondrial energy status affects nuclear control of basic cell decisions we have employed Affymetrix microarray-based transcriptional profiling of Drosophila S2 cells knocked down for the gene encoding subunit Va of the complex IV of the mitochondrial electron transport chain. The profiling data identifies up-regulation of glycolytic genes and metabolic studies confirm this increase in glycolysis. The transcriptional portrait which emerges implicates many signaling systems, including a p53 response, an insulin response, and up-regulation of conserved mitochondrial responses. This rich dataset provides many novel targets for further understanding the mechanism whereby the mitochondrion may direct cellular fate decisions. The data also provides a salient model of the shift of metabolism from a predominately oxidative state towards a predominately aerobic glycolytic state, and therefore provides a model of energy substrate management not unlike that found in cancer. Drosophila S2 cells were transfected with siRNA specific for either green flourescent protein (GFP) or cytochrome oxidase subunit va (COVA) thereby knocking down electron transport in the COVA transfectants

ORGANISM(S): Drosophila melanogaster

SUBMITTER: William Freije

PROVIDER: E-GEOD-32912 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression profiling of attenuated mitochondrial function identifies retrograde signals in Drosophila

Project description:Mitochondria are able to modulate cell state and fate during normal and pathophysiologic conditions through a nuclear mediated mechanism collectively termed as a retrograde response. Our previous studies in Drosophila have clearly established that progress through the cell cycle is precisely regulated by the intrinsic activity of the mitochondrion by specific signaling cascades mounted by the cell. As a means to further our understanding of how mitochondrial energy status affects nuclear control of basic cell decisions we have employed Affymetrix microarray-based transcriptional profiling of Drosophila S2 cells knocked down for the gene encoding subunit Va of the complex IV of the mitochondrial electron transport chain. The profiling data identifies up-regulation of glycolytic genes and metabolic studies confirm this increase in glycolysis. The transcriptional portrait which emerges implicates many signaling systems, including a p53 response, an insulin response, and up-regulation of conserved mitochondrial responses. This rich dataset provides many novel targets for further understanding the mechanism whereby the mitochondrion may direct cellular fate decisions. The data also provides a salient model of the shift of metabolism from a predominately oxidative state towards a predominately aerobic glycolytic state, and therefore provides a model of energy substrate management not unlike that found in cancer.

2012-05-20 | GSE32912 | GEO

Glycolytic preconditioning in astrocytes mitigates trauma-induced neurodegeneration

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Glycolytic preconditioning in astrocytes mitigates trauma-induced neurodegeneration

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Transcript level responses of Plasmodium falciparum to antimycin A

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2012-04-19 | E-GEOD-28625 | biostudies-arrayexpress

Transcript level responses of Plasmodium falciparum to antimycin A

2012-04-20 | GSE28625 | GEO

mRNA-sequencing of thyroid cancer cell lines

Project description:A metabolic hallmark of cancer identified by Warburg is the increased consumption of glucose and secretion of lactate, even in the presence of oxygen. Although many tumors exhibit increased glycolytic activity, most forms of cancer rely on mitochondrial respiration for tumor growth. We report here that Hürthle cell carcinoma of the thyroid (HTC) models harboring mitochondrial DNA-encoded defects in complex I of the mitochondrial electron transport chain exhibit impaired respiration and alterations in glucose metabolism. CRISPR-Cas9 pooled screening identified glycolytic enzymes as selectively essential in complex I-mutant HTC cells. We demonstrate in cultured cells and a PDX model that small molecule inhibitors of lactate dehydrogenase selectively induce an ATP crisis and cell death in HTC. This work demonstrates that complex I loss exposes fermentation as a therapeutic target in HTC and has implications for other tumors bearing mutations that irreversibly damage mitochondrial respiration.

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Pooled CRISPR-Cas9 screens for metabolic liabilities in Hurthle cell carcinoma

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

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Comparative proteomics of human visceral and subcutaneous adipocytes

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2016-08-01 | E-GEOD-74666 | biostudies-arrayexpress

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