Expression data from adult male Drosophila heads
Ontology highlight
ABSTRACT:
ORGANISM(S): Drosophila melanogaster
PROVIDER: GSE20202 | GEO | 2011/02/01
SECONDARY ACCESSION(S): PRJNA125711
REPOSITORIES: GEO
Similar Datasets
Project description:A Drosophila microRNA (dme-miR-14) is involved in regulating the levels of insulin-like peptides (ilps) from the neuronal insulin-producing cells (IPCs). This is crucial for regulation of fat content in adult flies. Finding the target of this microRNA is crucial for understanding the regulation of ilp gene expression. We used microarrays to identify genes that are upregulated specifically in the neuronal IPCs in the microRNA mutants. Drosophila adult head RNA was extracted and hybridized on Affymetrix microarrays. We reared animals from early larval stages in controlled growth and feeding conditions. RNA was extracted from 5-day-old adult males. We collected RNA from control, homozygous dme-miR-14 mutants and mutants expressing dme-miR-14 microRNA specifically in the IPCs (rescue). We were interested in genes that were upregulated in the mutants and were restored or reduced to control levels in the rescue condition. Two biological replicates per sample type were performed.
2011-02-01 | E-GEOD-20202 | biostudies-arrayexpress
Project description:Blattella germanica Insulin-like Peptides (ILPs)
| PRJEB23932 | ENA
Project description:Neuropeptides are secreted molecules that have conserved roles modulating many processes, including mood, reproduction, and feeding. Dysregulation of neuropeptide signaling is also implicated in neurological disorders such as epilepsy. However, much is unknown about the mechanisms regulating specific neuropeptides to mediate behavior. Here, we report that the expression levels of dozens of neuropeptides are up-regulated in response to circuit activity imbalance in C. elegans. acr-2 encodes a homolog of human nicotinic receptors, and functions in the cholinergic motoneurons. A hyperactive mutation, acr-2(gf), causes an activity imbalance in the motor circuit. We performed cell-type specific transcriptomic analysis and identified genes differentially expressed in acr-2(gf), compared to wild type. The most over-represented class of genes are neuropeptides, with insulin-like-peptides (ILPs) the most affected. Moreover, up-regulation of neuropeptides occurs in motor neurons, as well as sensory neurons. In particular, the induced expression of the ILP ins-29 occurs in the BAG neurons, which are previously shown to function in gas-sensing. We also show that this up-regulation of ins-29 in acr-2(gf) animals is activity-dependent. Our genetic and molecular analyses support cooperative effects for ILPs and other neuropeptides in promoting motor circuit activity in the acr-2(gf) background. Together, this data reveals that a major transcriptional response to motor circuit dysregulation is in up-regulation of multiple neuropeptides, and suggests that BAG sensory neurons can respond to intrinsic activity states to feedback on the motor circuit.
2019-10-22 | GSE139212 | GEO
Project description:Background Insulin signaling pathway is conserved from worms to humans. In Drosophila, three insulin-like peptides (dilps) are expressed in the insulin producing cells (IPCs) in the brain. In order to identify target genes of insulin signaling, the IPCs of female flies were destroyed during development by expressing apoptosis inducing factors reaper and head involution defective under control of the promoter region of dilp3. These insulin-deficient flies were analysed using high density microarrays. Results From the genes that appeared to be regulated in the absence of IPCs, the strongest difference was found for a gene involved in carbohydrate metabolism. Sequence analysis revealed that it is an alpha-glucosidase, which is able to break down disaccharides and/or glycogen. Conclusions We could identify an alpha-glucosidase, involved in carbohydrate metabolism, to be strongly affected in the context of decreased insulin signaling. The striking feature of this regulation was not only that it was the highest regulated, but it was the only gene regulated to this degree. Nutrient Conditions and Fly handling Experimental and control female flies were collected after hatching, then kept on fly maintenance food and separated from males after 11 days. After one day of recovery from carbon dioxide treatment, females were put in cages with PBS agar plates and supplied with yeast paste as only food source for 48 hours. Flies were shock frozen in liquid nitrogen and stored at - 80°C for further handling. Keywords: IPC knockout, 14 day old female flies, 48h yeast feeding
2008-02-27 | GSE10625 | GEO
Project description:The nervous system comprises diverse and highly specialized neuron-types, each expressing a unique set of genes that defines its functional properties. What molecular mechanisms generate diverse neuron types remains a central question in neuroscience. Our study of C. elegans chemosensory BAG neurons showed that a p38 MAP kinase (MAPK), PMK-3, is required for their proper differentiation and function (Brandt, J. and Ringstad, N. 2015). How p38 MAPKs function in neurodifferentiation is poorly understood. To better understand how pmk-3 promotes the BAG cell fate, we purified wild-type and pmk-3 mutant chemosensory BAG neurons and determined their transcriptomes using RNA-Seq. Expression of a number of genes that encode neuropeptides, including insulin-like peptides (ILPs), were up-regulated in pmk-3 mutant BAG neurons. Through analysis of mutations that restore expression of a BAG-fate marker to pmk-3 mutants, we additionally found that genes required for the release of neuropeptides, including UNC-31/CAPS, suppress pmk-3 mutant gene expression defects. These two observations suggested that the differentiation defects of pmk-3 mutants are associated with dysregulated release of peptide hormones. Indeed, we find that increased synthesis and release of ILPs from BAG during development causes a significant fraction of the gene expression and functional defects of pmk-3 mutant neurons. Together our data delineate a mechanism through which p38 MAPKs promote proper sensory neuron differentiation by inhibiting an autocrine insulin signal that represses expression of a BAG neuron fate. These findings reveal an unexpected role for insulin signaling in nervous system development and suggest that insulin-like factors are at the nexus of intrinsic genetic programs and extrinsic signaling mechanisms that regulate cell fate and neuronal differentiation.
2019-09-12 | GSE137267 | GEO
Project description:Background Insulin signaling pathway is conserved from worms to humans. In Drosophila, three insulin-like peptides (dilps) are expressed in the insulin producing cells (IPCs) in the brain. In order to identify target genes of insulin signaling, the IPCs of female flies were destroyed during development by expressing apoptosis inducing factors reaper and head involution defective under control of the promoter region of dilp3. These insulin-deficient flies were analysed using high density microarrays. Results From the genes that appeared to be regulated in the absence of IPCs, the strongest difference was found for a gene involved in carbohydrate metabolism. Sequence analysis revealed that it is an alpha-glucosidase, which is able to break down disaccharides and/or glycogen. Conclusions We could identify an alpha-glucosidase, involved in carbohydrate metabolism, to be strongly affected in the context of decreased insulin signaling. The striking feature of this regulation was not only that it was the highest regulated, but it was the only gene regulated to this degree. Nutrient Conditions and Fly handling Experimental and control female flies were collected after hatching, then kept on fly maintenance food and separated from males after 11 days. After one day of recovery from carbon dioxide treatment, females were put in cages with PBS agar plates and supplied with yeast paste as only food source for 48 hours. Flies were shock frozen in liquid nitrogen and stored at - 80°C for further handling. Keywords: IPC knockout, 14 day old female flies, 48h yeast feeding Insulin producing cell deficient flies were compared to control flies. Two independent biological repeats were performed. From the two repeats, 5 chips were hybridised, including dye swap Experimental and control female flies were collected after hatching, then kept on fly maintenance food and separated from males after 11 days. After one day of recovery from carbon dioxide treatment, females were put in cages with PBS agar plates and supplied with yeast paste as only food source for 48 hours. The microarray was scanned 3 times: low scan (suffix _L in data table) with a low amplification / intensity to avoid saturated spots for proper data analysis, high scan (suffix _H in data table) with a high amplification / intensity to detect also weak fluorescent spots which are missed in the low scan and medium scan which lies between high and low intensity and gives additional data points for subsequent calculations. Both copies and all hybridisation repeats were used for normalisation, VALUE therefore has the same value for these copies in all relevant hybridisations. For additional information see publication and web link. Keywords = insulin, aging, longevity, nutrient dependance Lot batch = FP7
2010-06-25 | E-GEOD-10625 | biostudies-arrayexpress
Project description:In fasted mammals, glucose homeostasis is maintained through activation of the cAMP responsive CREB coactivator TORC2, which stimulates the gluconeogenic program in concert with the forkhead transcription factor FOXO1. Here we show that starvation also triggers TORC activation in Drosophila, where it maintains energy balance by promoting the expression of CREB target genes in the brain. TORC mutant flies have reduced glycogen and lipid stores, and they are sensitive to starvation as well as oxidative stress. Neuronal TORC expression rescued starvation and oxidative stress sensitivity as well as CREB target gene expression in TORC mutants. During refeeding, increases in insulin signaling inhibited TORC activity in wild type flies by stimulating the Salt Inducible Kinase 2 (SIK2)-mediated phosphorylation and subsequent degradation of TORC. Depletion of neuronal SIK2 increased TORC activity and enhanced resistance to starvation and oxidative stress in adult flies. As disruption of insulin signaling, either by ablation of insulin-producing cells (IPCs) or by mutation of the insulin receptor adaptor gene chico, also increased TORC activity, our results illustrate the importance of an insulin-regulated pathway in brain that promotes energy balance in Drosophila. Experiment Overall Design: Male fly heads were collected after 24h fasting, and RNA was extracted using RNAeasy kit.
2008-10-20 | E-GEOD-10546 | biostudies-arrayexpress
Project description:Animals change developmental fates in response to external cues. In the nematode Caenorhabditis elegans, unfavorable environmental conditions induce a state of diapause known as dauer by inhibiting the conserved DAF-2 insulin-like signaling (ILS) pathway through incompletely understood mechanisms. We previously established a role for the C. elegans dosage compensation protein DPY-21 in the control of dauer arrest and DAF-2 ILS. Here we show that dosage compensation acts through the histone H4 lysine 20 methyltransferase SET-4 to promote dauer arrest in part by repressing the X-linked ins-9 gene, which encodes a new agonist insulin-like peptide (ILP) expressed specifically in the paired ASI sensory neurons that are required for dauer bypass. ins-9 repression in dauer-constitutive mutants requires DPY-21, SET-4, and the FoxO transcription factor DAF-16, which is the main target of DAF-2 ILS. In contrast, autosomal genes encoding major agonist ILPs that promote reproductive development are not repressed by DPY-21, SET-4, or DAF-16/FoxO. Our results implicate the dosage compensation machinery as a sensory rheostat that reinforces developmental fates in response to environmental cues by modulating autocrine and paracrine DAF-2 ILS.
2017-02-28 | GSE89295 | GEO
Project description:Intracellular Ca2+ release through the Inositol 1,4,5-Triphosphate Receptor (InsP3R) is a feature of all multicellular organisms in which it shapes the temporal and spatial aspects of calcium signaling in cells, affecting several developmental and physiological processes. Mutants in the InsP3R gene of Drosophila (itpr) exhibit a range of defects which include growth defects and larval lethality.The Drosophila Insulin-like peptides (ILPs) are encoded by multigene families that are expressed in the brain and other tissues. Upon secretion, these peptides likely serve as hormones, neurotransmitters, and growth factors. In Drosophila melanogaster, molecular genetic studies have revealed Drosophila ILPs as elements of a conserved insulin signaling pathway, and as in other animal models, it appears to play a key role in metabolism, growth, reproduction, and aging. Previous work from our group has shown that InsP3R function can be rescued by ectopically expressing InsP3R in dilp cells or can be compensated by altering the activity of Sarco-Endoplasmic Reticulum Calcium-ATPase (SERCA). To understand the molecular basis of larval lethality and growth defect in Drosophila InsP3R mutants and to decipher possible cross talk of itpr gene with other signaling pathways we have carried out genome wide microarray experiments. We have compared the transcript profiles of i) itpr mutant larvae and wild type larvae, ii) dilp rescue larvae with itpr mutant larvae iii) itpr and SERCA double mutant larvae with itpr mutant larvae. By this we have identified genes whose levels are altered in itpr mutants and are restored towards wild type in dilp rescue larvae with itpr mutant larvae and itpr and SERCA double mutants. Our experiments help in identify genes that are regulated by changes in intracellular Ca2+ in the context of larval viability may contribute to the better understanding of the major human pathologies caused by calcium misbalance or by dysregulation of the insulin/IGF pathway.
2012-06-02 | GSE29736 | GEO
Project description:Intracellular Ca2+ release through the Inositol 1,4,5-Triphosphate Receptor (InsP3R) is a feature of all multicellular organisms in which it shapes the temporal and spatial aspects of calcium signaling in cells, affecting several developmental and physiological processes. Mutants in the InsP3R gene of Drosophila (itpr) exhibit a range of defects which include growth defects and larval lethality.The Drosophila Insulin-like peptides (ILPs) are encoded by multigene families that are expressed in the brain and other tissues. Upon secretion, these peptides likely serve as hormones, neurotransmitters, and growth factors. In Drosophila melanogaster, molecular genetic studies have revealed Drosophila ILPs as elements of a conserved insulin signaling pathway, and as in other animal models, it appears to play a key role in metabolism, growth, reproduction, and aging. Previous work from our group has shown that InsP3R function can be rescued by ectopically expressing InsP3R in dilp cells or can be compensated by altering the activity of Sarco-Endoplasmic Reticulum Calcium-ATPase (SERCA). To understand the molecular basis of larval lethality and growth defect in Drosophila InsP3R mutants and to decipher possible cross talk of itpr gene with other signaling pathways we have carried out genome wide microarray experiments. We have compared the transcript profiles of i) itpr mutant larvae and wild type larvae, ii) dilp rescue larvae with itpr mutant larvae iii) itpr and SERCA double mutant larvae with itpr mutant larvae. By this we have identified genes whose levels are altered in itpr mutants and are restored towards wild type in dilp rescue larvae with itpr mutant larvae and itpr and SERCA double mutants. Our experiments help in identify genes that are regulated by changes in intracellular Ca2+ in the context of larval viability may contribute to the better understanding of the major human pathologies caused by calcium misbalance or by dysregulation of the insulin/IGF pathway. The 8x60k array AMADID: 27326 slide was scanned immediately by PerkinElmer Scan array Gx Microarray scanner. The Scan array software (PerkinElmer) was used for grid wise normalization of array images. Three were used with Mutant, three for Dilp Rescue and two for Kum Rescue experiments . The data was analysed by GeneSpring GX Agilent . The differential expression was considered if the Log 2 mean of at least -1 for the down regulated genes and +1 for the upregulated genes. We considered only the genes that were reproducible from biological triplicates for Mutant, biological treplicates for Dilp Rescue and biological duplicates for Kum Rescue.
2012-06-01 | E-GEOD-29736 | biostudies-arrayexpress