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Omics score: 40

Genome-wide maps of metabolic labeled RNA in Drosophila S2 cells.

ABSTRACT: We report the application of ultrashort metabolic labeling of RNA for high-throughput profiling of RNA processing in Drosophila S2 cells. Overall design: Examination of 3 different labeling timepoints in Drosophila S2 cells.

INSTRUMENT(S): Illumina HiSeq 2000 (Drosophila melanogaster)

SUBMITTER: Karen Adelman

PROVIDER: GSE93763 | GEO | 2018-01-08

SECONDARY ACCESSION(S): PRJNA362313

REPOSITORIES: GEO

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Publications

The kinetics of pre-mRNA splicing in the Drosophila genome and the influence of gene architecture.

Pai Athma A AA Henriques Telmo T McCue Kayla K Burkholder Adam A Adelman Karen K Burge Christopher B CB

eLife 20171227

Production of most eukaryotic mRNAs requires splicing of introns from pre-mRNA. The splicing reaction requires definition of splice sites, which are initially recognized in either intron-spanning ('intron definition') or exon-spanning ('exon definition') pairs. To understand how exon and intron length and splice site recognition mode impact splicing, we measured splicing rates genome-wide in Drosophila, using metabolic labeling/RNA sequencing and new mathematical models to estimate rates. We fou ...[more]

PMID: 29280736

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9-(S)-HODE treatment of Drosophila S2 cells

Project description:Timecourse of 9-(S)-HODE treatment of Drosophila S2 cells. 9-(S)-HODE is an oxygenated metabolite of the abundant, 18 carbon, omega-6 PUFA linoleic acid. To discriminate how omega-6 PUFAs affect meta-inflammation S2 cells were with 10uM for 12 and 24hrs and microarrays performed to identify downstream transcriptional targets

2018-08-12 | E-MTAB-6253 | BioStudies

ChIP-chip profiles of MLE, MSL3 and MOF in Drosophila S2 cells

Project description:ChIP-chip profiles of MLE, MSL3 and MOF in Drosophila S2 cells MLE, MSL3 amd MOF ChIP in Drosophila S2 cells. 1-5 biological replicates per experiment. dye-swaps as indicated in sample description

2012-12-11 | E-GEOD-37863 | BioStudies

Pseudomonas exotoxin kills Drosophila S2 cells via apoptosis.

Project description:Pseudomonas exotoxin A (PE) is cytotoxic for eukaryotic cells because it enters cells by receptor-mediated endocytosis, translocates to the cell cytosol and ADP-ribosylates elongation factor 2 (EF2). However, the interaction of this toxin with eukaryotic cells and the mechanism of PE-mediated cell death have not been extensively characterized. The feasibility of carrying out a genome-wide RNAi screen, makes Drosophila melanogaster S2 cells as a good model system to identify essential genes in PE-mediated cytotoxicity, provided a suitable multi-well assay is developed. Here, using the alamarBlue viability assay, we show that Drosophila S2 cells are sensitive to PE at picomolar concentrations and that toxin treatments provoke an increase in caspase activity. This prompted us to use RNAi to characterize the mechanism of cell death. Results indicated that PE-mediated death of S2 cells was dependent on the presence of diphthamide, the post translational modification of EF2, and on the presence of Drice, the terminal caspase of insect cells. RNAi to drice or chemical inhibition of caspase action by z-VAD-fmk protected cells from PE-mediated death. Protection from death by RNAi or z-VAD-fmk did not interfere with toxin delivery to the cytosol leading to inhibition of protein synthesis. Using a convenient alamarBlue assay, our data confirms the cytotoxicity of PE for S2 cells and establishes apoptosis as the mode of PE-mediated death. This confirms the suitability of Drosophila cells as a convenient and simple model to elucidate the role of specific genes and proteins required for PE action.

2010-01-01 | S-EPMC3431163 | BioStudies

Use of Drosophila S2 cells as a model for studying Ehrlichia chaffeensis infections.

Project description:Ehrlichia chaffeensis is an obligate intracellular bacterium and the causative agent of human monocytic ehrlichiosis. Although this pathogen grows in several mammalian cell lines, no general model for eukaryotic cellular requirements for bacteria replication has yet been proposed. We found that Drosophila S2 cells are permissive for the growth of E. chaffeensis. We saw morulae (aggregates of bacteria) by microscopy, detected the E. chaffeensis 16S rRNA gene by reverse transcriptase PCR, and used immunocytochemistry to detect E. chaffeensis in S2 and mammalian cells. Bacteria grown in S2 cells reinfected mammalian macrophages. S2 cells were made nonpermissive for E. chaffeensis through incubation with lipopolysaccharide. Our results demonstrate that S2 cells are an appropriate system for studying the pathogenesis of E. chaffeensis. The use of a Drosophila system has the potential to serve as a model system for studying Ehrlichia due to its completed genome, ease of genetic manipulation, and the availability of mutants.

2008-01-01 | S-EPMC2268305 | BioStudies

Drosophila S2 cells are non-permissive for vaccinia virus DNA replication following entry via low pH-dependent endocytosis and early transcription.

Project description:Vaccinia virus (VACV), a member of the chordopox subfamily of the Poxviridae, abortively infects insect cells. We have investigated VACV infection of Drosophila S2 cells, which are useful for protein expression and genome-wide RNAi screening. Biochemical and electron microscopic analyses indicated that VACV entry into Drosophila S2 cells depended on the VACV multiprotein entry-fusion complex but appeared to occur exclusively by a low pH-dependent endocytic mechanism, in contrast to both neutral and low pH entry pathways used in mammalian cells. Deep RNA sequencing revealed that the entire VACV early transcriptome, comprising 118 open reading frames, was robustly expressed but neither intermediate nor late mRNAs were made. Nor was viral late protein synthesis or inhibition of host protein synthesis detected by pulse-labeling with radioactive amino acids. Some reduction in viral early proteins was noted by Western blotting. Nevertheless, synthesis of the multitude of early proteins needed for intermediate gene expression was demonstrated by transfection of a plasmid containing a reporter gene regulated by an intermediate promoter. In addition, expression of a reporter gene with a late promoter was achieved by cotransfection of intermediate genes encoding the late transcription factors. The requirement for transfection of DNA templates for intermediate and late gene expression indicated a defect in viral genome replication in VACV-infected S2 cells, which was confirmed by direct analysis. Furthermore, VACV-infected S2 cells did not support the replication of a transfected plasmid, which occurs in mammalian cells and is dependent on all known viral replication proteins, indicating a primary restriction of DNA synthesis.

2011-01-01 | S-EPMC3039670 | BioStudies

Differential metabolism of neonicotinoids by Myzus persicae CYP6CY3 stably expressed in Drosophila S2 cells.

Project description:The peach-potato aphid, Myzus persicae, is a serious crop pest that has developed imidacloprid resistance, mainly through overexpression of CYP6CY3. Here, we established a metabolic assay using Drosophila S2 cells that stably expressed CYP6CY3. We found that CYP6CY3 showed metabolic activity against imidacloprid, as well as acetamiprid, clothianidin, and thiacloprid, but had no activity against dinotefuran. Our study suggested that stable gene expression in Drosophila S2 cells is useful for examining which insecticide is metabolized by P450 monooxygenases.

2019-01-01 | S-EPMC6718358 | BioStudies

Transcriptional profiling of Drosophila S2 cells in early response to Drosophila C virus.

Project description:BACKGROUND:The innate immune response like phagocytosis, encapsulation and antimicrobial peptide (AMP) production often occur in the early stage of host-pathogen interactions in Drosophila melanogaster. To investigate the Drosophila early immune response to Drosophila C virus, we characterized the DCV infection-response transcriptome of Drosophila Schneider 2 (S2) cells at one hour post inoculation. METHOD:The total RNA was extracted from treated S2 cells by using Trizol reagent and then analyzed by CapitalBio Corp for Drosophila GeneChip (Affymetrix) assay. Then the results of signaling pathway and protein interaction about these genes were analyzed by MAS 3.0 software. RESULTS:Most significantly affected genes (656 genes) by DCV infection were regulated as the same way in inactivated DCV treatment, but inactivated white spot syndrome virus (WSSV) showed a different transcriptome. DCV infection up-regulated the expression levels of 275 genes and down-regulated that of 442 genes significantly and some affected genes were related to phagocytosis. DCV infection activated the JAK/STAT pathway by 1 hour post incubation. The Imd pathway was activated and transcriptional induction of antimicrobial peptides (AMPs) from this pathway was enhanced by 1 hour post incubation. But the Toll pathway was not activated like Imd pathway and the expression levels of AMPs from this pathway was reduced. In addition, most pattern-recognition receptors were inhibited and the antiviral RNAi pathway was not activated in the early stage of DCV infection. CONCLUSIONS:In conclusion, the present study demonstrates that DCV infection may activate phagocytosis, JAK/STAT pathway and Imd pathway in the early host-virus interactions. These results indicate that DCV is capable of activating or inhibiting some immune responses in the host cells and these changes would be vital for virus entry and replication.

2013-01-01 | S-EPMC3704779 | BioStudies

Light-Induced Protein Clustering for Optogenetic Interference and Protein Interaction Analysis in Drosophila S2 Cells.

Project description:Drosophila Schneider 2 (S2) cells are a simple and powerful system commonly used in cell biology because they are well suited for high resolution microscopy and RNAi-mediated depletion. However, understanding dynamic processes, such as cell division, also requires methodology to interfere with protein function with high spatiotemporal control. In this research study, we report the adaptation of an optogenetic tool to Drosophila S2 cells. Light-activated reversible inhibition by assembled trap (LARIAT) relies on the rapid light-dependent heterodimerization between cryptochrome 2 (CRY2) and cryptochrome-interacting bHLH 1 (CIB1) to form large protein clusters. An anti-green fluorescent protein (GFP) nanobody fused with CRY2 allows this method to quickly trap any GFP-tagged protein in these light-induced protein clusters. We evaluated clustering kinetics in response to light for different LARIAT modules, and showed the ability of GFP-LARIAT to inactivate the mitotic protein Mps1 and to disrupt the membrane localization of the polarity regulator Lethal Giant Larvae (Lgl). Moreover, we validated light-induced co-clustering assays to assess protein-protein interactions in S2 cells. In conclusion, GFP-based LARIAT is a versatile tool to answer different biological questions, since it enables probing of dynamic processes and protein-protein interactions with high spatiotemporal resolution in Drosophila S2 cells.

2019-01-01 | S-EPMC6406598 | BioStudies

Expression in aneuploid Drosophila S2 cells.

Project description:Extensive departures from balanced gene dose in aneuploids are highly deleterious. However, we know very little about the relationship between gene copy number and expression in aneuploid cells. We determined copy number and transcript abundance (expression) genome-wide in Drosophila S2 cells by DNA-Seq and RNA-Seq. We found that S2 cells are aneuploid for >43 Mb of the genome, primarily in the range of one to five copies, and show a male genotype ( approximately two X chromosomes and four sets of autosomes, or 2X;4A). Both X chromosomes and autosomes showed expression dosage compensation. X chromosome expression was elevated in a fixed-fold manner regardless of actual gene dose. In engineering terms, the system "anticipates" the perturbation caused by X dose, rather than responding to an error caused by the perturbation. This feed-forward regulation resulted in precise dosage compensation only when X dose was half of the autosome dose. Insufficient compensation occurred at lower X chromosome dose and excessive expression occurred at higher doses. RNAi knockdown of the Male Specific Lethal complex abolished feed-forward regulation. Both autosome and X chromosome genes show Male Specific Lethal-independent compensation that fits a first order dose-response curve. Our data indicate that expression dosage compensation dampens the effect of altered DNA copy number genome-wide. For the X chromosome, compensation includes fixed and dose-dependent components.

2010-01-01 | S-EPMC2826376 | BioStudies

Drosophila CTCF is required for Fab-8 enhancer blocking activity in S2 cells.

Project description:CTCF is a conserved transcriptional regulator with binding sites in DNA insulators identified in vertebrates and invertebrates. The Drosophila Abdominal-B locus contains CTCF binding sites in the Fab-8 DNA insulator. Previous reports have shown that Fab-8 has enhancer blocking activity in Drosophila transgenic assays. We now confirm the enhancer blocking capability of the Fab-8 insulator in stably transfected Drosophila S2 cells and show this activity depends on the Fab-8 CTCF binding sites. Furthermore, knockdown of Drosophila CTCF by RNAi in our stable cell lines demonstrates that CTCF itself is critical for Fab-8 enhancer blocking.

2007-01-01 | S-EPMC2694738 | BioStudies

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