Drosophila melanogaster
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-37148
PROVIDER: PRJNA158425 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcriptome Profiling following Neuronal and Glial Expression of ALS-linked SOD1 in Drosophila
2015-09-28 | E-GEOD-37148 | ExpressionAtlas
Project description:Amyotrophic Lateral Sclerosis (ALS) is generally a late onset neurodegenerative disease. Mutations in the Cu/Zn superoxide dismutase 1 (SOD1) gene accounts for approximately 20% of familial ALS and 2% of all ALS cases. Although a number of hypothesis have been proposed to explain mutant SOD1 toxicity, the molecular mechanisms of the disease remain unclear. SOD1 linked ALS is thought to function in a non-cell autonomous manner such that the motoneurons are critical for the onset and glia contribute to the progress of the disease. To dissect the roles of motoneurons and glia, we used the Gal4-UAS system to determine gene expression changes following the expression of mutant human SOD1 (G85R) selectively in either motoneurons or glia, and concurrently in motoneurons and glia of flies. We conducted a microarray on young (5 days old) and old (45 days old) flies expressing G85R in these cell types and identified a number of genes involved in a variety of processes. The candidate genes identified by this screen may help elucidate the individual and combined contributions of motoneurons and glial cells in ALS. We used microarrays to evaluate the transcriptional profile of 5 day old and 45 day old flies expressing mutant human SOD1 (G85R) in a tissue specific manner in motoneurons, glia, and together in motoneurons and glia and compared the expression to flies expressing wild-type drosophila SOD1 controls. The Gal4-UAS system was used to drive tissue expression of either mutant human SOD1 (G85R) or wild-type drosophila SOD1 (dSOD1) in flies. Flies containing either the motoneuronal driver, D42-Gal4, the glial driver, M1B-Gal4, or the combined motoneuronal and glial drivers, D42+M1B-Gal4 were crossed to flies containing either mutant human SOD1, UAS-G85R, or wild-type drosophila SOD1, UAS-dSOD1, as a control. Adult male progeny were collected within 24 hours after eclosion and aged to 5 (5d) and 45 (45d) days old. Groups of 10 flies were maintained in vials of cornmeal agar food and transferred to fresh food every 5-7 days. For each Gal4-UAS line and each age, 3 biological replicates consisting of 40 whole flies were flash frozen in liquid nitrogen and used to isolate total RNA, for a total of 36 samples.
2012-06-30 | E-GEOD-37148 | biostudies-arrayexpress
Project description:Amyotrophic Lateral Sclerosis (ALS) is generally a late onset neurodegenerative disease. Mutations in the Cu/Zn superoxide dismutase 1 (SOD1) gene accounts for approximately 20% of familial ALS and 2% of all ALS cases. Although a number of hypothesis have been proposed to explain mutant SOD1 toxicity, the molecular mechanisms of the disease remain unclear. SOD1 linked ALS is thought to function in a non-cell autonomous manner such that the motoneurons are critical for the onset and glia contribute to the progress of the disease. To dissect the roles of motoneurons and glia, we used the Gal4-UAS system to determine gene expression changes following the expression of mutant human SOD1 (G85R) selectively in either motoneurons or glia, and concurrently in motoneurons and glia of flies. We conducted a microarray on young (5 days old) and old (45 days old) flies expressing G85R in these cell types and identified a number of genes involved in a variety of processes. The candidate genes identified by this screen may help elucidate the individual and combined contributions of motoneurons and glial cells in ALS. We used microarrays to evaluate the transcriptional profile of 5 day old and 45 day old flies expressing mutant human SOD1 (G85R) in a tissue specific manner in motoneurons, glia, and together in motoneurons and glia and compared the expression to flies expressing wild-type drosophila SOD1 controls.
2012-07-01 | GSE37148 | GEO
Project description:Transcriptional profiling of Drosophila wing pouch following CR32027 RNAi
| PRJNA238066 | ENA
Project description:ChIP-seq study analysing adult Drosophila melanogaster head, glial, neuronal and fat body, as well as embryonic RNA pol II and H2A.v binding by employing the GAL4-UAS system to generate GFP-fusion proteins and ChIP-seq
2013-08-25 | E-MTAB-1117 | biostudies-arrayexpress
Project description:Transcriptional profiling of Drosophila melanogaster photoreceptors following nuclei affinity enrichment
| PRJNA360105 | ENA
Project description:Y-linked rDNA deletions in Drosophila melanogaster
| PRJNA138155 | ENA
Project description:Multifunctional glial support by Semper cells in the Drosophila retina
| PRJNA362350 | ENA
Project description:Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disorder with limited therapeutic interventions. We identified the cGAS-STING-NFκB pathway as a dual therapeutic target that combats both neuronal degeneration and neurotoxic glial activity in ALS. Utilizing SOD1-mutant human iPSC-differentiated motor neurons(hiPSC-MNs) and microglia(hiPSC-MGs), we demonstrated that ALS hiPSC-MGs displayed a pronounced proinflammatory phenotype, characterized by significant inflammatory marker elevation (NLRP3 increased 0.66-fold, secreted IL-1β elevated 2.85-fold compared to controls) and compromised phagocytic capacity (48% reduction in bioparticle uptake). Concurrently, ALS hiPSC-MNs exhibit DNA damage, activating STING-NFκB signaling and triggering caspase-3-mediated apoptosis. Notably, co-culture experiments revealed that inflammatory hiPSC-MGs substantially increased neuronal apoptosis, indicating a toxic intercellular communication mechanism mediated through STING-NFκB signaling. Pharmacological inhibition of Bruton's tyrosine kinase (BTK) - a critical upstream regulator of STING activation - effectively suppressed this inflammatory cascade. This intervention reduced DNA damage in ALS hiPSC-MNs by 61.4% and restored microglial phagocytic function to approximately 87.2% of normal levels. In vivo studies with SOD1-G93A ALS mice demonstrated that BTK inhibitor treatment significantly improved motor performance, extended median survival (183 days versus 158 days in untreated controls), and mitigated neuropathological progression. The treatment enhanced motor neuron survival, reduced microgliosis and astrogliosis, and modulated the PI3K-AKT-mTOR pathway without disrupting autophagy-lysosome dynamics. Our study presents a translational therapeutic strategy that simultaneously addresses neuron-intrinsic and glial-mediated mechanisms in ALS, providing a compelling rationale for repurposing BTK inhibitors in future ALS clinical trials.
2026-06-13 | GSE299859 | GEO