Dynamic regulation of chromatin signatures during Drosophila embryonic glial differentiation [ChIP-Seq]
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ABSTRACT:
ORGANISM(S): Drosophila melanogaster
PROVIDER: GSE83376 | GEO | 2016/11/20
SECONDARY ACCESSION(S): PRJNA325733
REPOSITORIES: GEO
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Project description:Expression profiles of affinity-purified nuclei of GBs and glias from the Drosophila embryos.
2016-11-20 | GSE83375 | GEO
Project description:Dynamic regulation of chromatin signatures during Drosophila embryonic glial differentiation
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Project description:While circadian rhythm disruption may promote neurodegenerative disease, how aging and neurodegenerative pathology impact circadian gene expression patterns in different brain cell types is unknown. Here, we used translating ribosome affinity purification methods to define the circadian translatomes of astrocytes, microglia, and bulk cerebral cortex, in healthy mouse brain and in the settings of amyloid-beta plaque pathology or aging. Our data reveal that glial circadian translatomes are highly cell type-specific and exhibit profound, context-dependent reprogramming of rhythmic transcripts in response to amyloid pathology or aging. Transcripts involved in glial activation, immunometabolism, and proteostasis, as well as nearly half of all Alzheimer Disease (AD)-associated risk genes, displayed circadian oscillations, many of which were altered by pathology. Amyloid-related differential gene expression was also dependent on time of day. Thus, circadian rhythms in gene expression are cell- and context dependent and provide important insights into glial gene regulation in health, AD, and aging.
2024-06-26 | GSE261698 | GEO
Project description:The goals of this research are three-fold: (i) One is to identify genetic changes associated with tumorgenesis that interfere with the ability of transformed glial cells to differentiate. This is connected with (ii) our analysis of the regulation of differentiation in normal glial progentor cells, as only by understanding this in normal cells can we understand what is occurring when differentiation fails in transformed versions of the same cells. (iii) The third is to identify the molecular basis for the greater resistance of transformed glial progenitor cells to chemotherapeutic agents as compared with normal glial progenitor cells. Thus, analysis of the populations provided will yield data crucial to two of our central areas of research, as awarded by NINDS in "Oligodendrocytes & precursors: toxicity of chemotherapy" (5R01NS044701), and "Low-level toxicant perturbation of neural cell function" (1R01ES012708). Our ability to work with essentially unlimited numbers of primary progenitor cells and transformed derivatives of these cells offers one of the few systems in which side-by-side comparison of normal and transformed cells at both the biochemical and molecular levels is possible. Using defined cell populations, expression profiles will be compared to reveal changes in cell type specific markers and regulatory factors associated with transformation. In addition, retention of markers despite transformation may enable identification of new markers useful in the diagnosis of glial tumors. Transformation of glial progenitor cells is associated both with loss of the proteins required for normal differentiation and with an inability to normally activate proteins that function in differentiation control. By side-by-side analysis of gene expression in normal and transformed glial progenitor cells, and analysis of the response to inducers of differentiation in each these populations, we will identify candidate regulators critical in the control of normal differentiation. Identification of these regulators will also provide clues as to overcome the blockade of differentiation that occurs in glial cancers (which represent the majority of adult brain tumors). RNA will be isolated from two separate preparations of glial progenitors. Preparation of purified populations has been described in multiple of our previous publications (Mayer, M. et al. (1994) Development 120, 142-153; Mayer-Pröschel, M. et al. (1997) Neuron 19, 773-785; Rao, M. and Mayer-Pröschel, M. (1997) Dev. Biology 188, 48-63). Total RNA from purified cell cultures will be extracted in a two step process. RNA will first be extracted by dounce homogenization in phenol/guanidine isothiocyonate solution (Trizol, Invitrogen, California) followed by isopropanol precipitation. Contaminating traces of DNA and protein will then be removed by silica-based affinity chromatography and Dnase treatment (NucleoSpin RNA Purification system, Clontech, California). Depending on the cell type, 5x105 cells will typically yield 5-15µg of high quality RNA (OD260/280=2.1 at pH7.5). In order to determine purity and molecular weight distribution, samples will be routinely tested on a Agilent Bioanalyzer. cDNA will be generated from total RNA and then be submitted to one round of amplification and labeling using the messageAmp system (Ambion). Probes are then hybridized to the Affymerix Rat 230 (A/B or 2.0) GeneChip expression array. Array data will be processed using the Micro Array Suite 5.0 (MAS, Affymetrix). .Cel files containing normalized, relative expression data for all genes tested will be used for downstream statistical analysis.
2008-06-16 | E-GEOD-9763 | biostudies-arrayexpress
Project description:We employ multi-step affinity purification followed by high-throughput sequencing to determine the location of EJC complexes assembled on a cellular transcriptome in Drosophila S2 cells, finding 6% of the intron-containing genes were not associated with EJCs, and within genes with multiple introns, only specific exon-exon junctions assembled an EJC. RIP-Seq, 3 samples
2014-11-04 | E-GEOD-33475 | biostudies-arrayexpress
Project description:Gliogenesis in the Drosophila CNS occurs during embryogenesis and also during the postembryonic larval stages. Several glial subtypes are generated in the postembryonic CNS through the proliferation of differentiated glial cells. The genes and molecular pathways that regulate glial proliferation in the postembryonic CNS are poorly understood. In this study we aimed to use gene expressing profiling of CNS tissue enriched in glia to identify genes expressed in glial cells in the postembryonic CNS. We used microarrays to compare the gene expression profiles from the larval CNS of animals that had increased numbers of glial cells to identify genes that are expressed in glia. RNA was purified from the late third instar larval CNS from control larvae, or larvae expressing an activated form of the FGF receptor (Hlt[ACT]), or overexpressing the insulin receptor (InR) in glial cells using the glial specific driver repoGal4 to increase the number of glial cells and generate CNS tissue enriched in glia.
2013-04-24 | E-GEOD-46317 | biostudies-arrayexpress
Project description:We employ multi-step affinity purification followed by high-throughput sequencing to determine the location of EJC complexes assembled on a cellular transcriptome in Drosophila S2 cells, finding 6% of the intron-containing genes were not associated with EJCs, and within genes with multiple introns, only specific exon-exon junctions assembled an EJC.
2014-11-04 | GSE33475 | GEO
Project description:We use a metabolic labeling strategy for directly measuring nucleosome turnover to examine the effect of doxorubicin on chromatin dynamics in squamous cell carcinoma cell lines derived from genetically defined mice. We find that doxorubicin enhances nucleosome turnover around gene promoters, and turnover correlates with gene expression level. Keywords: Chromatin affinity-purification on microarray
2013-04-19 | GSE43753 | GEO
Project description:The goals of this research are three-fold: (i) One is to identify genetic changes associated with tumorgenesis that interfere with the ability of transformed glial cells to differentiate. This is connected with (ii) our analysis of the regulation of differentiation in normal glial progentor cells, as only by understanding this in normal cells can we understand what is occurring when differentiation fails in transformed versions of the same cells. (iii) The third is to identify the molecular basis for the greater resistance of transformed glial progenitor cells to chemotherapeutic agents as compared with normal glial progenitor cells. Thus, analysis of the populations provided will yield data crucial to two of our central areas of research, as awarded by NINDS in "Oligodendrocytes & precursors: toxicity of chemotherapy" (5R01NS044701), and "Low-level toxicant perturbation of neural cell function" (1R01ES012708). Our ability to work with essentially unlimited numbers of primary progenitor cells and transformed derivatives of these cells offers one of the few systems in which side-by-side comparison of normal and transformed cells at both the biochemical and molecular levels is possible. Using defined cell populations, expression profiles will be compared to reveal changes in cell type specific markers and regulatory factors associated with transformation. In addition, retention of markers despite transformation may enable identification of new markers useful in the diagnosis of glial tumors. Transformation of glial progenitor cells is associated both with loss of the proteins required for normal differentiation and with an inability to normally activate proteins that function in differentiation control. By side-by-side analysis of gene expression in normal and transformed glial progenitor cells, and analysis of the response to inducers of differentiation in each these populations, we will identify candidate regulators critical in the control of normal differentiation. Identification of these regulators will also provide clues as to overcome the blockade of differentiation that occurs in glial cancers (which represent the majority of adult brain tumors). RNA will be isolated from two separate preparations of glial progenitors. Preparation of purified populations has been described in multiple of our previous publications (Mayer, M. et al. (1994) Development 120, 142-153; Mayer-Pröschel, M. et al. (1997) Neuron 19, 773-785; Rao, M. and Mayer-Pröschel, M. (1997) Dev. Biology 188, 48-63). Total RNA from purified cell cultures will be extracted in a two step process. RNA will first be extracted by dounce homogenization in phenol/guanidine isothiocyonate solution (Trizol, Invitrogen, California) followed by isopropanol precipitation. Contaminating traces of DNA and protein will then be removed by silica-based affinity chromatography and Dnase treatment (NucleoSpin RNA Purification system, Clontech, California). Depending on the cell type, 5x105 cells will typically yield 5-15µg of high quality RNA (OD260/280=2.1 at pH7.5). In order to determine purity and molecular weight distribution, samples will be routinely tested on a Agilent Bioanalyzer. cDNA will be generated from total RNA and then be submitted to one round of amplification and labeling using the messageAmp system (Ambion). Probes are then hybridized to the Affymerix Rat 230 (A/B or 2.0) GeneChip expression array. Array data will be processed using the Micro Array Suite 5.0 (MAS, Affymetrix). .Cel files containing normalized, relative expression data for all genes tested will be used for downstream statistical analysis. Keywords: other
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