Project description:The COP9 signalosome (CSN), an eight-subunit protein complex, is conserved in all higher eukaryotes. CSN intersects the ubiquitin-proteasome pathway, modulating signaling pathways controlling various aspects of development. We are using Drosophila as a model system to elucidate the function of this important complex. Transcriptome data was generated for four csn mutants, sampled at three developmental time points. Our results are highly reproducible, being confirmed using two different experimental setups that entail different microarrays and different controls. Our results indicate that the CSN acts as a transcriptional repressor during Drosophila development, resulting in achronic gene expression in the csn mutants. "Time shift" analysis with the publicly-available Drosophila transcriptome data indicates that genes repressed by the CSN are normally induced primarily during late embyogenesis, or during metamorphosis. These temporal shifts are likely due to the roles of the CSN in regulating transcription factors. A null mutation in CSN subunit 4, and hypomorphic mutations in csn5 lead to more severe defects than seen in the csn5null mutants strain, suggesting that CSN5 carries only some of the CSN function. Keywords: time course csn mutants

2007-04-12 | GSE7303 | GEO

Drosophila melanogaster

Project description:Transcriptome analysis of Drosophila Kr-h1 mutants

| PRJNA339575 | ENA

Drosophila melanogaster

Project description:Differential gene expression analysis in the larval heart of Drosophila

| PRJNA112895 | ENA

Drosophila melanogaster

Project description:Gene expression profiling of dMyc null Drosophila larvae

| PRJNA103647 | ENA

RNA-Seq of Drosophila melanogaster Cdk12-null mutants versus control

Project description:In a forward genetic screen, we have previously identified a null mutant of Cdk12 that results in alterations in actin dynamics, the axon initial segment and electrophysiology in Drosophila melanogaster. To decipher how Cdk12 may be having these effects, we extracted RNA from pooled Drosophila heads and compared Cdk12-null mutants to controls at the transcriptome level.

2023-01-01 | E-MTAB-12090 | biostudies-arrayexpress

Chronic sleep loss sensitizes Drosophila melanogaster to nitrogen stress

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

Drosophila melanogaster

Project description:Drosophila brain gene expression between wildtype and miR-34 null flies

| PRJNA142725 | ENA