Drosophila melanogaster
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA247816 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1288440.fastq.gz | Fastqsanger.gz | |||
| SRR1288441.fastq.gz | Fastqsanger.gz | |||
| SRR1288434_1.fastq.gz | Fastqsanger.gz | |||
| SRR1288434_2.fastq.gz | Fastqsanger.gz | |||
| SRR1288435_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
Similar Datasets
Project description:The exon junction complex controls transposable element activity by ensuring faithful splicing of the piwi transcript
| PRJNA255082 | ENA
Project description:Transposable elements can drive genome evolution, but their enhanced activity is detrimental to the host and therefore must be tightly regulated. The piwi-interacting small RNAs (piRNAs) pathway is critically important for transposable element regulation, by inducing transcriptional silencing or post-transcriptional decay of mRNAs. We show that piRNAs and piRNA biogenesis components regulate pre-mRNA splicing of P transposable element transcripts in vivo, leading to the production of the non-transposase-encoding mature mRNA isoform in germ cells. Unexpectedly, we show that the piRNA pathway components do not act to reduce P-element transposon transcript levels during P-M hybrid dysgenesis, a syndrome that affects germline development in Drosophila. Instead, splicing regulation is mechanistically achieved in concert with piRNA-mediated changes to repressive chromatin states, and relies on the function of the Piwi-piRNA complex proteins Asterix/Gtsf1 and Panoramix/Silencio, as well as Heterochromatin Protein 1a (Su(var)205/HP1a). Furthermore, we show that this machinery, together with the piRNA Flamenco cluster, not only controls the accumulation of Gypsy retrotransposon transcripts but also regulates splicing of Gypsy mRNAs in cultured ovarian somatic cells, a process required for the production of infectious particles that can lead to heritable transposition events. Our findings identify splicing regulation as a new role and essential function for the Piwi pathway in protecting the genome against transposon mobility, and provide a model system for studying the role of chromatin structure in modulating alternative splicing during development.
2017-12-06 | GSE103582 | GEO
Project description:The exon junction complex (EJC) is a highly conserved ribonucleoprotein complex which binds RNAs at a late stage of the splicing reaction and remains associated following export to the cytoplasm. This complex is involved in several cellular post-transcriptional processes including mRNA localization, translation and degradation. The EJC plays an additional role in the splicing of a subset of genes in Drosophila and in human cells but the underlying mechanism remains to be elucidated. Here, we have found a novel function for the EJC and its splicing subunit RnpS1 in preventing transposon accumulation in both Drosophila germline and surrounding follicular cells. This function is mediated specifically through the control of the splicing of the piwi transcript. In absence of RnpS1 one of the piwi intron is retained. This intron contains a weak 5’ splice site as well as degenerate transposon fragments, reminiscent of heterochromatic introns. In addition, we identified a small A/T rich region, which alters its polypyrimidine tract (PPT) and confers the RnpS1’s dependency. Finally, we showed that the removal of this intron by RnpS1 requires the initial splicing of the flanking introns, suggesting a model in which the EJC facilitates the splicing of challenging introns following its initial deposition to adjacent exon junctions. In total there are 4 different conditions. Comparisons were made between piwi mutant vs control piwi and rnps1 KD vs controls RnpS1
2014-09-08 | E-GEOD-57710 | biostudies-arrayexpress
Project description:Splicing of pre-mRNAs results in the deposition of the exon junction complex (EJC) upstream of exon-exon boundaries. The EJC plays crucial post-splicing roles in export, translation, localization and nonsense-mediated decay of mRNAs. It also aids faithful splicing of pre-mRNAs containing large introns, albeit via an unknown mechanism. Here, we show that the core EJC plus the accessory factors RnpS1 and Acinus aid in definition and efficient splicing of neighboring introns. This requires prior deposition of the EJC in close proximity either from an upstream or downstream splicing event. If present in isolation, EJC-dependent introns are splicing-defective also in wildtype cells. Interestingly, the most affected intron belongs to the piwi locus, which explains the reported transposon de-silencing in EJC-depleted Drosophila ovaries. We propose that the dependency of splicing on the EJC is exploited as a means to control the temporal order of splicing events. Our observations provide a powerful basis to dissect the molecular events that underlie the role of the EJC in splicing. Analysis of splicing defects in 3 knockdowns (siGFP [control], siACN, siTSU) in Drosohpila OSCs. PolyA RNA (biological duplicates) and total-RNA was sequenced on a Illumina HiSeq2000 in PE50 mode.
2014-12-04 | E-GEOD-58830 | biostudies-arrayexpress
Project description:Splicing of pre-mRNAs results in the deposition of the exon junction complex (EJC) upstream of exon-exon boundaries. The EJC plays crucial post-splicing roles in export, translation, localization and nonsense-mediated decay of mRNAs. It also aids faithful splicing of pre-mRNAs containing large introns, albeit via an unknown mechanism. Here, we show that the core EJC plus the accessory factors RnpS1 and Acinus aid in definition and efficient splicing of neighboring introns. This requires prior deposition of the EJC in close proximity either from an upstream or downstream splicing event. If present in isolation, EJC-dependent introns are splicing-defective also in wildtype cells. Interestingly, the most affected intron belongs to the piwi locus, which explains the reported transposon de-silencing in EJC-depleted Drosophila ovaries. We propose that the dependency of splicing on the EJC is exploited as a means to control the temporal order of splicing events. Our observations provide a powerful basis to dissect the molecular events that underlie the role of the EJC in splicing.
2014-12-04 | GSE58830 | GEO
Project description:The exon junction complex (EJC) is a highly conserved ribonucleoprotein complex which binds RNAs during splicing and remains associated with them following export to the cytoplasm. While the role of this complex in mRNA localization, translation and degradation has been well characterized, its mechanism of action in splicing a subset of Drosophila and human transcripts remains to be elucidated. Here, we describe a novel function for the EJC and its splicing subunit RnpS1 in preventing transposon accumulation in both Drosophila germline and surrounding somatic follicle cells. This function is mediated specifically through the control of piwi transcript splicing, where in the absence of RnpS1 the fourth intron of piwi is retained. Within this intron the polypyrimidine tract is disrupted by a transposon-adjacent A/T-rich sequence that confers dependence on RnpS1. Finally, we demonstrate that RnpS1-dependent removal of this intron requires splicing of the flanking introns, suggesting a model in which the EJC facilitates the splicing of weak introns following its initial deposition at adjacent exon junctions. These data demonstrate a novel role for the EJC in regulating piwi intron excision and provide a mechanism for its function during splicing. Small-RNA libraries from two control samples and four knockdowns in germline or somatic tissues of the Drosophila melanogaster ovary.
2014-08-14 | E-GEOD-59327 | biostudies-arrayexpress
Project description:This series represents 52 tissues hybridized across 5 different chip patterns. Probes were placed at every exon-exon junction in each transcript. Keywords = junction alternate splicing oligonucleotide Keywords: parallel sample
2003-12-19 | GSE740 | GEO
Project description:The exon junction complex (EJC) is a highly conserved ribonucleoprotein complex which binds RNAs during splicing and remains associated with them following export to the cytoplasm. While the role of this complex in mRNA localization, translation and degradation has been well characterized, its mechanism of action in splicing a subset of Drosophila and human transcripts remains to be elucidated. Here, we describe a novel function for the EJC and its splicing subunit RnpS1 in preventing transposon accumulation in both Drosophila germline and surrounding somatic follicle cells. This function is mediated specifically through the control of piwi transcript splicing, where in the absence of RnpS1 the fourth intron of piwi is retained. Within this intron the polypyrimidine tract is disrupted by a transposon-adjacent A/T-rich sequence that confers dependence on RnpS1. Finally, we demonstrate that RnpS1-dependent removal of this intron requires splicing of the flanking introns, suggesting a model in which the EJC facilitates the splicing of weak introns following its initial deposition at adjacent exon junctions. These data demonstrate a novel role for the EJC in regulating piwi intron excision and provide a mechanism for its function during splicing.
2014-08-14 | GSE59327 | GEO
Project description:This series represents 52 tissues hybridized across 5 different chip patterns. Probes were placed at every exon-exon junction in each transcript. Keywords = junction alternate splicing oligonucleotide Keywords: parallel sample. This dataset is part of the TransQST collection.
2003-12-19 | E-GEOD-740 | biostudies-arrayexpress
Project description:Transposable elements, known colloquially as “jumping genes,” constitute approximately 45% of the human genome. Cells utilize epigenetic defenses to limit transposable element jumping, including formation of silencing heterochromatin and generation of piwi-interacting RNAs (piRNAs), small RNAs that facilitate clearance of transposable element transcripts. Here we identify transposable element activation as a key mediator of neuronal death in tauopathies, a group of neurodegenerative disorders, including Alzheimer’s disease, that are pathologically characterized by deposits of tau protein in the brain. Mechanistically, we find that heterochromatin decondensation and reduction of piwi/piRNAs drive transposable element activation in tauopathy. Using genetic and pharmacological approaches in a Drosophila melanogaster model of tauopathy, we provide evidence for a causal relationship between pathogenic tau-induced heterochromatin decondensation, piwi/piRNA depletion, active transposable element obilization, and neurodegeneration. We further report a significant increase in transcripts of the endogenous retrovirus class of transposable elements in human Alzheimer’s disease and progressive supranuclear palsy, suggesting that transposable element dysregulation is conserved in human tauopathy. Taken together, our data identify heterochromatin decondensation, piwi/piRNA depletion and consequent transposable element activation as a novel, pharmacologically targetable, mechanistic driver of neurodegeneration in tauopathy.
2018-07-04 | GSE115606 | GEO