Drosophila melanogaster
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA146539 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Chromatin profiling of Drosophila CNS subpopulations identifies active transcriptional enhancers
| PRJNA326060 | ENA
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. 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
2012-05-19 | E-GEOD-32912 | biostudies-arrayexpress
Project description:Drosophila HNF4 promotes glucose-stimulated insulin secretion and increased mitochondrial function in adults [ChIP-seq]
| PRJNA297626 | ENA
Project description:Drosophila HNF4 promotes glucose-stimulated insulin secretion and increased mitochondrial function in adults [RNA-seq]
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Project description:Drosophila CNS mitochondrial DNA dysfunction microarray
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Project description:Complete mitochondrial genome of Drosophila melanogaster
| PRJNA13669 | ENA
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
Project description:Stresses that target mitochondrial function lead to altered transcriptional responses for 100-1000s of genes genome wide, and are signalled via retrograde communication pathways within the cell. rao2 mutants contain a mutation in the NAC family transcription factor ANAC017 and cannot induce stress responsive genes (such as the mitochondrial alternative oxidase 1a) in response to mitochondrial dysfunction. We sought to define the global gene network regulated through RAO2 function in response to mitochondrial stress (mimicked through treatment of plants with antimycin A - a specific inhibitor of complex III in the mitochondrial electron transfer chain), and non-specific stress signals such as hydrogen peroxide. We have defined global stress responses that are positively and negatively mediated by RAO2 function, and show that greater than 80% of transcripts that are differentially regulated under H2O2 stress require proper functioning of ANAC017 for a normal stress responses. We used Affymetrix microarray to characterise global gene expression profiles for mutant plants with compromised mitochondrial retrograde signalling (rao2 mutants), to define the genome wide transcriptional network regulated through RAO1 function under mitochondrial stress and hydrogen peroxide stress. rao2 EMS lines, independent T-DNA knock-out lines for ANAC017 (anac017-1), ANAC017 gain of function mutants (anac017-2) and wild type seedlings were grown for 14 days, the optimal stage as defined by forward genetic screens that identifed rao2 mutants. Seedlings were grown on GamborgB5 plates and treated by spraying plants with 50 µM antimycin A (an elicitor of mitochondrial retrograde signalling) or 20mM hydrogen peroxide while mock control samples were sprayed with deionised water. Samples were collected after 3hr of treatment for global expression profiling.
2013-01-30 | E-GEOD-41136 | biostudies-arrayexpress
Project description:Presynaptic efficacy can be modulated by retrograde control mechanisms, but the nature of these complex signaling systems remain obscure. Some studies have suggested that retrograde synaptic communication requires new protein synthesis in the postsynaptic compartment, yet the putative translational targets that mediate this signaling are enigmatic. To gain insight into the retrograde mechanisms that stabilize synaptic transmission at the neuromuscular junction, we have developed and optimized a tissue-specific ribosome profiling approach in Drosophila. We first demonstrate the ability of this technology to define genome-wide translational regulations that could not be inferred from transcription, and validate the superior sensitivity of ribosome profiling over conventional translational profiling. We then leverage this technology to test the relative contributions of transcriptional, translational, and post-translational mechanisms in the postsynaptic muscle that orchestrate the retrograde control of presynaptic function. Surprisingly, we find no changes in transcription or translation are necessary to enable retrograde homeostatic signaling. Rather, post-translational mechanisms appear to ultimately gate instructive retrograde communication. Finally, we find that a global increase in translation induces adaptive responses in both transcription and translation of protein chaperones and degradation factors to promote cellular proteostasis. Together, this demonstrates the power of ribosome profiling to define transcriptional, translational, and post-translational mechanisms driving retrograde signaling during adaptive plasticity.
2017-11-06 | GSE99920 | GEO
Project description:Gene expression in a Drosophila model of mitochondrial disease
| PRJNA108371 | ENA