Drosophila melanogaster
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA392170 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We performed a transcriptome analysis of the larval VNC in kdm5 WT, kdm5[L854F] and enzymatically inactive kdm5[JmjC] in order to identify genes contributing to the phenotypes observed in the mutants' neuromuscular junction (NMJ). We found that inactivation of the catalytic activity in kdm5[JmjC] causes dysregulation of genes related to glutamate metabolism while the mutation L854F leads to dysregulation of genes involved in microtubule cytoskeleton dynamics. We also found a group of genes dysregulated in both mutants that likely explain a common NMJ phenotype.
2021-03-16 | GSE159298 | GEO
Project description:RNA-seq analysis of de larval ventral nerve cord (VNC) from kdm5[L854F] and enzymatically inactive kdm5[JmjC*]
| PRJNA668325 | ENA
Project description:The goal of this study was to generate a Drosophila model of intellectual disability caused by mutations in kdm5. RNA-seq was used to define the transcriptional defects of a mutation in Drosophila that is analogous to a human intellectual disability-associated allele, kdm5[A512p]. These data revealed a total of 1609 dysregulated genes, 778 of which were upregulated and 831 were downregulated. To determine whether these transcriptional defects were due to the loss of KDM5-induced histone demethylation, we also carried out RNA-seq from a enzymatic inactive strain, kdm5[Jmjc*]. These data revealed a striking similarity between the two datasets and suggest that the primary defect of KDM5[A512P] is loss of histone demethylase activity.
2018-12-31 | GSE100578 | GEO
Project description:Expression data from adult male Drosophila heads
| PRJNA125711 | ENA
Project description:To determine which genes affected by loss of KDM5 in adults were direct targets, we carried out KDM5 ChIP-seq analyses. To valide this data, we utilized a previously generated fly strain in which the sole source of KDM5 is from a transgene expressing an HA tagged form of KDM5 expressed under the control of its endogenous promoter. Comparing genome-wide gene expression and KDM5 binding analyses in Drosophila adults, we demonstrate the primary function of KDM5 in adults is to activate gene expression KDM5. To investigate the link between KDM5 and H3K4me3, we carried out anti-H3K4me3 ChIP-seq from wildtype adults . Genome-wide, KDM5 and H3K4me3 peaks showed a similar distribution, with both peaking at the transcription start site (TSS) showed a striking overlap with the presence of H3K4me3. Examination of KDM5 binding and histone H3K4me3 modifications in drosophila adults
2015-12-22 | E-GEOD-70589 | biostudies-arrayexpress
Project description:Aging in heads from adult Drosophila males, w118 strain
| PRJNA104727 | ENA
Project description:RNA-seq analyses of kdm5 mutant flies and wt flies under normal condition and oxidative stress
| PRJNA289117 | ENA
Project description:<p>Chronic sleep loss profoundly impacts metabolic health and shortens lifespan, but studies of the mechanisms involved have focused largely on acute sleep deprivation. To identify metabolic consequences of chronically reduced sleep, we conducted unbiased metabolomics on heads of three adult Drosophila short-sleeping mutants with very different mechanisms of sleep loss: fumin (fmn), redeye (rye), and sleepless (sss). Common features included elevated ornithine and polyamines, with lipid, acyl-carnitine, and TCA cycle changes suggesting mitochondrial dysfunction. Studies of excretion demonstrate inefficient nitrogen elimination in adult sleep mutants, likely contributing to their polyamine accumulation. Increasing levels of polyamines, particularly putrescine, promote sleep in control flies but poison sleep mutants. This parallels the broadly enhanced toxicity of high dietary nitrogen load from protein in chronically sleep-restricted Drosophila, including both sleep mutants and flies with hyper-activated wake-promoting neurons. Together, our results implicate nitrogen stress as a novel mechanism linking chronic sleep loss to adverse health outcomes-and perhaps for linking food and sleep homeostasis at the cellular level in healthy organisms.</p>
2023-03-18 | MTBLS3318 | MetaboLights
Project description:To determine which genes affected by loss of KDM5 in adults were direct targets, we carried out KDM5 ChIP-seq analyses. To valide this data, we utilized a previously generated fly strain in which the sole source of KDM5 is from a transgene expressing an HA tagged form of KDM5 expressed under the control of its endogenous promoter. Comparing genome-wide gene expression and KDM5 binding analyses in Drosophila adults, we demonstrate the primary function of KDM5 in adults is to activate gene expression KDM5. To investigate the link between KDM5 and H3K4me3, we carried out anti-H3K4me3 ChIP-seq from wildtype adults . Genome-wide, KDM5 and H3K4me3 peaks showed a similar distribution, with both peaking at the transcription start site (TSS) showed a striking overlap with the presence of H3K4me3.
2015-12-22 | GSE70589 | GEO
Project description:We used long-oligonucleotide microarrays to investigate whether alternative splicing in Drosophila is regulated in a sex-, stage-, or tissue-specific manner. To examine sex-specific splicing, we compared gene expression profiles of male and female pupae 12 hours after pupariation. To examine stage-specific splicing, we compared expression profiles of mixed-sex, 0-24 hour old embryos and mixed-sex, 12 hour old pupae. To examine tissue-specific splicing, we compared expression profiles of adult male heads and abdomens 24-48 hours after eclosion. To examine tissue-specific splicing, we compared expression profiles of adult male heads and abdomens at 24-48 hours after eclosion. Keywords: tissue-specific expression profiles
2007-06-22 | GSE5190 | GEO