E-MTAB-9805
Ontology highlight
ABSTRACT:
PROVIDER: E-MTAB-9805 | ExpressionAtlas | 2020-12-09
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:Stress and neuronal activity during a critical period regulate odorant receptor expression in Drosophila Melanogaster
| PRJEB41507 | ENA
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:Neural functions and circuit establishment are characterized by intricate crosstalk among multiple cell types during critical periods. Impeding or delaying the crosstalk results in abnormal neural functions and neurodevelopmental disorders. However, the lack of robust mouse models to study the crosstalk between astrocytes and neurons thus renders unclear the implications of impeding such interactions. Here we found that Egfr knockout led to the absence of astrocytes during the critical period of neuronal maturation, with recovery observed in adult mice, providing an exceptional opportunity to investigate the consequences of delaying crosstalk between astrocytes and neurons. We show that, in the absence of Egfr, glial progenitor cells are unable to migrate outwardly, exhibiting a rounded and smooth morphology. This phenomenon arises as a direct consequence of the impaired Egfr-pERK-Epb41l2 signaling axis, leading to delayed communication between astrocytes and neurons. This delay results in reduced neuronal dendritic complexity and decreased neuronal excitability (due to damage to the Sema6a-Plxna2/4 receptor pair between astrocytes and neurons during the critical period), ultimately leading to the manifestation of depressive-like behaviors in adult mice.
2024-11-19 | PXD058068 |
Project description:Ayurvedic drug formulations Bacopa monnieri and Centella asiatica are known to have neuroprotective effects. These have been traditionally used in the treatment of Alzhemeir’s disease, and other neurological deficits. Using pan neuronal Aβ42 model of Drosophila melanogaster, a mass spectrometry based quantitative proteomic analysis platform was used to generate the data on proteins altered in response to the Aβ42 toxicity and restoration of altered proteins by consumption of aqueous extracts of two Ayurvedic drug formulations Bacopa monnieri and Centella asiatica aqueous extract. Quantitative proteomic analysis resulted in 0.67 million mass spectra corresponding to 2,59,168 peptide-spectrum matches (PSM) mapping to 24,305 non- redundant peptides corresponding to 11,480 Drosophila melanogaster proteins. Proteins were filtered for >3 PSMs, resulting in 9,540 proteins. Flies expressing Aβ42 significantly altered 517 proteins which were involved in maintaining essential neuronal functions. Supplementing flies with Bacopa monnieri or Centella asiatica extract commonly rescued 224 proteins from Aβ42 toxicity, moreover, extract supplemented group significantly altered proteins which were additionally supporting neuronal maintenance in flies with Aβ42 stress.
2021-11-25 | PXD027101 | Pride
Project description:Transcriptional regulation by Store-operated Calcium Entry (SOCE) is well studied in non-excitable cells. However, the role of SOCE has been poorly documented in neuronal cells with more complicated calcium dynamics. Previous reports demonstrated a requirement of neuronal SOCE for Drosophila flight. We identified the early pupal stage to be critical and used RNA-sequencing to identify SOCE mediated gene expression changes in the developing Drosophila pupal nervous system. We down-regulated dStim, the endoplasmic reticular calcium sensor and a principal component of SOCE in the nervous system for a 24h period during pupal development, and compared wild type and knockdown transcriptional profiles, immediately after knockdown as well as after a 36h recovery period. We found that dStim knockdown altered the expression of a number of genes. We also characterized one of the down-regulated genes, Ral for its role in flight. Thus, we identify neuronal SOCE as a mechanism that regulates expression of a number of genes during the development of the pupal nervous system. These genes can be further studied in the context of pupal nervous system development.
2017-03-21 | GSE89168 | GEO
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. Keywords: Fasting-induced gene expression
2008-07-04 | GSE10546 | GEO
Project description:Complete metamorphosis of holometabolous insects is a complex biological process characterized by profound morphological, physiological, and transcriptional changes. To reveal the temporal dynamics of gene expression during this critical developmental transition, a detailed analysis of the developmental transcriptomes of two Drosophila species, Drosophila melanogaster and Drosophila virilis, was conducted. We confirm partial recapitulation of the embryonic transcriptional program in pupae, but instead of the traditional hourglass model, which posits maximal conservation at mid-embryonic stages, at different stages of pupae we observe a more complicated pattern of alternating low and high diversity, resembling an inverted hourglass, or "spindle". This observation challenges the notion of a singular conserved phylotypic period during holometabola ontogeny and underscores the complexity of developmental processes during complete metamorphosis. Notably, recently formed genes (specific to insects) exhibit pronounced expression peaks during mid-pupal development, underscoring their potential role in developmental transitions.
2024-06-17 | GSE269951 | GEO
Project description:Auditory experience drives neural circuit refinement during auditory circuit development, but little is known about the genetic regulation of this developmental process. The primary auditory cortex (A1) exhibits a critical period for thalamocortical connectivity between postnatal days P12 and P15, during which tone exposure alters the tonotopic topography of A1. We hypothesized that a coordinated, multicellular transcriptional program governs this window for patterning of the auditory cortex. To test this idea, we generated a multicellular map of gene expression by performing droplet-based, single-nucleus RNA sequencing (snRNA-seq) of A1 across three developmental time points spanning the tonotopic critical period (P10, P15, P20). We also tone-reared mice (7 kHz pips) during the 3-day critical period and carried out snRNA-seq of A1 at P15 and P20. Using semi-supervised clustering and marker genes, we identified and profiled neuronal (glutamatergic and GABAergic) and non-neuronal (oligodendrocytes, microglia, astrocytes, and endothelial) cell types in A1 under these different conditions to identify candidate genes that might regulate auditory critical period plasticity. By comparing normally reared and tone-reared mice, we identified hundreds of genes in both glutamatergic and GABAergic cells with altered expression as a result of sensory manipulation in the critical period. In addition, we identified previously unknown effects of developmental tone exposure on interneuron developmental trajectories. This single-cell transcriptomic resource of the developing auditory cortex will provide a powerful discovery platform for future characterization of mediators of tonotopic plasticity.
2020-04-01 | GSE140883 | GEO
Project description:We report the 4C-seq data and ChIP-seq to study Shep regulation of chromatin looping. We also reported ATAC-seq and CUT&Tag data on sorted neurons that reveal chromatin accessibility and states during the neuronal remodeling of Drosophila melanogaster
2021-08-30 | GSE154645 | GEO
Project description:Brain postnatal development is characterized by critical periods of experience dependent remodeling. Maturation of local circuits inhibitory neurons terminate this period of enhanced plasticity. Astroglial cells are known to influence excitatory and inhibitory synaptic transmission as well as network activity through active signaling mechanisms. Although these can be developmentally regulated, the role of astrocytes in the timing of post-natal critical period is unknown. Here we show in the visual cortex that astrocytes con-trol the maturation of inhibitory neurons and thereby closure of the critical period. We uncover a novel underlying pathway involving regulation of the extracellular matrix that allows interneurons maturation via astroglial connexin signaling. We find that timing of the critical period closure is controlled by a marked upregulation of the astroglial protein connexin 30 that inhibits expression of the matrix degrading enzyme MMP9 through the RhoA-GTPase pathway. Our results thus demonstrate that astrocytes not only influ-ence neuronal activity but are also key elements in the experience–dependent wiring of brain circuits. Therefore, astrocytes represent a new cellular partner to consider in our understanding of the post-natal shaping of neuronal activities, hence providing a new target to alleviate malfunctions associated to im-paired closure of the critical period and settling of synaptic circuits.
2022-05-12 | PXD020448 | Pride