Drosophila melanogaster
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA110905 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR014268.fastq.gz | Fastqsanger.gz | |||
| SRR014269.fastq.gz | Fastqsanger.gz | |||
| SRR014270.fastq.gz | Fastqsanger.gz | |||
| SRR014271.fastq.gz | Fastqsanger.gz | |||
| SRR014272.fastq.gz | Fastqsanger.gz |
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Project description:The piRNA pathway controls transposon expression in animal germ cells, thereby ensuring genome stability over generations. piRNAs are maternally deposited and required for proper transposon silencing in adult offspring. However, a long-standing question in the field is the precise function of maternally deposited piRNAs and its associated factors during embryogenesis. Here, we probe the spatio-temporal expression patterns of several piRNA pathway components during early stages of development. Amongst those, factors required for transcriptional gene silencing (TGS) showed ubiquitous abundance in somatic and pole cells throughout the first half of embryogenesis. We further analysed the transcriptomes of various embryo stages and correlated these with the presence of selected chromatin marks. We found that a number of transposon families show bursts of transcription during early embryonic stages. Transposons heavily targeted by maternally deposited piRNAs accumulated repressive chromatin marks following their spike in expression. Furthermore, depletion of maternally deposited Piwi protein in early embryos resulted in increased expression of transposons targeted by inherited piRNAs and was accompanied by a strong loss of repressive chromatin marks at coding sequences. Overall, our data suggests a pivotal role for the piRNA pathway in transposon defence during Drosophila embryogenesis in somatic cells.
2021-07-26 | PXD022409 | Pride
Project description:Transposons evolve rapidly and can mobilize and trigger genetic instability. piRNAs silence these genome pathogens, but it is unclear how the piRNA pathway adapts to new transposons. In Drosophila piRNAs, encoded by heterochromatic clusters are maternally deposited in the embryo. Paternally inherited P-element transposons thus escape silencing and trigger a genetic instability and sterility. We show that this syndrome, termed P-M hybrid dysgenesis, also disrupts the piRNA biogenesis machinery and activates resident transposons. As dysgenic hybrids age, however, fertility is restored, P-elements are silenced, and P-element piRNAs are produced de novo. In addition, the piRNA biogenesis machinery is restored and resident elements are silenced. Significantly, new resident transposons insertions accumulate in piRNA clusters, and these new insertions are transmitted to progeny with high fidelity, produce novel piRNAs, and are associated with reduced transposition. P-M hybrid dysgenesis thus leads to heritable changes in chromosome structure that appear to enhance transposon silencing.
2011-12-23 | GSE31813 | GEO
Project description:The piRNA pathway controls transposon expression in animal germ cells, thereby ensuring genome stability over generations. piRNAs are maternally deposited and required for proper transposon silencing in adult offspring. However, a long-standing question in the field is the precise function of maternally deposited piRNAs and its associated factors during embryogenesis. Here, we probe the spatio-temporal expression patterns of several piRNA pathway components during early stages of development. Amongst those, factors required for transcriptional gene silencing (TGS) showed ubiquitous abundance in somatic and pole cells throughout the first half of embryogenesis. We further analyzed the transcriptomes of various embryo stages and correlated these with the presence of selected chromatin marks. We found that a number of transposon families show bursts of transcription during early embryonic stages. Transposons heavily targeted by maternally deposited piRNAs accumulated repressive chromatin marks following their spike in expression. Furthermore, depletion of maternally deposited Piwi protein in early embryos resulted in increased expression of transposons targeted by inherited piRNAs and was accompanied by a strong loss of repressive chromatin marks at coding sequences. Overall, our data suggests a pivotal role for the piRNA pathway in transposon defence during Drosophila embryogenesis in somatic cells.
2021-07-22 | GSE160778 | GEO
Project description:Transposons evolve rapidly and can mobilize and trigger genetic instability. piRNAs silence these genome pathogens, but it is unclear how the piRNA pathway adapts to new transposons. In Drosophila piRNAs, encoded by heterochromatic clusters are maternally deposited in the embryo. Paternally inherited P-element transposons thus escape silencing and trigger a genetic instability and sterility. We show that this syndrome, termed P-M hybrid dysgenesis, also disrupts the piRNA biogenesis machinery and activates resident transposons. As dysgenic hybrids age, however, fertility is restored, P-elements are silenced, and P-element piRNAs are produced de novo. In addition, the piRNA biogenesis machinery is restored and resident elements are silenced. Significantly, new resident transposons insertions accumulate in piRNA clusters, and these new insertions are transmitted to progeny with high fidelity, produce novel piRNAs, and are associated with reduced transposition. P-M hybrid dysgenesis thus leads to heritable changes in chromosome structure that appear to enhance transposon silencing. 3 replicates of each sample (Har 2-4 days, w1 x Har 2-4 days, w1 x Har 21 days), total RNA samples hybridized to tiling array.
2011-12-23 | E-GEOD-31813 | biostudies-arrayexpress
Project description:Heterochromatin, representing the silenced state of transcription, largely consists of transposon-enriched and highly repetitive sequences. Implicated in heterochromatin formation and transcriptional silencing in Drosophila are PIWI and repeat-associated small interfering RNAs (rasiRNAs). Despite this, the role of PIWI in rasiRNA expression and heterochromatic silencing remains unknown. Here we report the identification and characterization of 12,903 PIWI-interacting RNAs (piRNAs) in Drosophila, demonstrating that rasiRNAs represent a subset of piRNAs. Keywords: PIWI, piRNA, epigenetic regulation, heterochromatin
2007-10-25 | GSE9138 | GEO
Project description:Heterochromatin, representing the silenced state of transcription, largely consists of transposon-enriched and highly repetitive sequences. Implicated in heterochromatin formation and transcriptional silencing in Drosophila are PIWI and repeat-associated small interfering RNAs (rasiRNAs). Despite this, the role of PIWI in rasiRNA expression and heterochromatic silencing remains unknown. Here we report the identification and characterization of 12,903 PIWI-interacting RNAs (piRNAs) in Drosophila, demonstrating that rasiRNAs represent a subset of piRNAs. Keywords: PIWI, piRNA, epigenetic regulation, heterochromatin PIWI-associated small RNA cDNA library was sequenced for one time by high-throughput 454 pyrosequencing. Putative small RNA sequences were extracted and BLAST against the Drosophila melanogaster genome release 5. Presented here is a list of non-redundant PIWI-associated small RNAs, which have at least one genome match determined by BLASTn.
2007-10-24 | E-GEOD-9138 | biostudies-arrayexpress
Project description:Drosophila Piwi-family proteins have been implicated in transposon control. Here, we examine piwi-interacting RNAs (piRNAs) associated with each Drosophila Piwi protein and find that Piwi and Aubergine bind RNAs that are predominantly antisense to transposons, whereas Ago3 complexes contain predominantly sense piRNAs. As in mammals, the majority of Drosophila piRNAs are derived from discrete genomic loci. These loci comprise mainly defective transposon sequences, and some have previously been identified as master regulators of transposon activity. Our data suggest that heterochromatic piRNA loci interact with potentially active, euchromatic transposons to form an adaptive system for transposon control. Complementary relationships between sense and antisense piRNA populations suggest an amplification loop wherein each piRNA-directed cleavage event generates the 5’ end of a new piRNA. Thus, sense piRNAs, formed following cleavage of transposon mRNAs, may enhance production of antisense piRNAs, complementary to active elements, by directing cleavage of transcripts from master control loci. Keywords: small RNA libraries from Drosophila ovaries
2007-03-08 | GSE6734 | GEO
Project description:In plants and mammals, small RNAs indirectly mediate epigenetic inheritance by specifying cytosine methylation. Here, we find that small RNAs themselves serve as vectors for epigenetic information. Crosses between Drosophila strains that differ in the presence of a particular transposon can produce sterile progeny, a phenomenon called hybrid dysgenesis. This phenotype manifests itself only if the transposon is paternally inherited, suggesting maternal transmission of a factor that maintains fertility. In both P- and I-element-mediated hybrid-dysgenesis models, daughters show a markedly different content of piRNAs targeting each element, depending upon its parent of origin. Such differences persist from fertilization through adulthood. This indicates that maternally deposited piRNAs are crucial for mounting an effective silencing response and that a lack of maternal piRNA inheritance underlies hybrid dysgenesis. Mappers table contains all of the sequences in our libraries that map to the drosophila genome (release 5) Nonmappers table contains all of the sequences in our libraries that do not map to the drosophila genome(release 5)
2008-11-28 | GSE13081 | GEO
Project description:In plants and mammals, small RNAs indirectly mediate epigenetic inheritance by specifying cytosine methylation. Here, we find that small RNAs themselves serve as vectors for epigenetic information. Crosses between Drosophila strains that differ in the presence of a particular transposon can produce sterile progeny, a phenomenon called hybrid dysgenesis. This phenotype manifests itself only if the transposon is paternally inherited, suggesting maternal transmission of a factor that maintains fertility. In both P- and I-element-mediated hybrid-dysgenesis models, daughters show a markedly different content of piRNAs targeting each element, depending upon its parent of origin. Such differences persist from fertilization through adulthood. This indicates that maternally deposited piRNAs are crucial for mounting an effective silencing response and that a lack of maternal piRNA inheritance underlies hybrid dysgenesis. Mappers table contains all of the sequences in our libraries that map to the drosophila genome (release 5) Nonmappers table contains all of the sequences in our libraries that do not map to the drosophila genome(release 5) 15 small RNA libraries were generated from total RNA of Drosophila melanogaster ovarian and embryo tissues and analyzed for this study
2008-11-28 | E-GEOD-13081 | biostudies-arrayexpress
Project description:RNA interference systems depend on the synthesis of small RNA precursors whose sequences define the target spectrum of these silencing pathways. The Drosophila Heterochromatin Protein 1 (HP1) variant Rhino permits transcription of PIWI-interacting RNA (piRNA) precursors within transposon-rich heterochromatic loci in germline cells. Current models propose that Rhino’s specific chromatin occupancy at piRNA source loci is determined by histone marks and maternally inherited piRNAs, but also imply the existence of other, undiscovered specificity cues. Here, we identify a member of the diverse family of zinc finger associated domain (ZAD)-C2H2 proteins, Kipferl, as critical Rhino cofactor in ovaries. By binding to guanosine-rich DNA motifs and interacting with the Rhino chromodomain, Kipferl recruits Rhino to specific loci and stabilizes it on chromatin. In kipferl mutant flies, Rhino is lost from most of its target chromatin loci and instead accumulates on pericentromeric satellite arrays, resulting in decreased levels of transposon targeting piRNAs and impaired fertility. Our findings reveal that DNA sequence, in addition to the H3K9me3 mark, determines the identity of piRNA source loci and provide insight into how Rhino might be caught in the crossfire of genetic conflicts.
2022-05-15 | GSE202467 | GEO