PIWI-piRNA pathway mediated transposon repression in Hydra somatic stem cells
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ABSTRACT:
PROVIDER: PRJNA558896 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9909310.fastq.gz | Fastqsanger.gz | |||
| SRR9909311.fastq.gz | Fastqsanger.gz | |||
| SRR9909312.fastq.gz | Fastqsanger.gz | |||
| SRR9909313.fastq.gz | Fastqsanger.gz | |||
| SRR9909314.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
Similar Datasets
Project description:Transposable elements (TEs) can damage genomes, thus organisms employ a variety of mechanisms to repress TE expression. The PIWI-piRNA pathway is a small RNA pathway that represses TE expression in the germline of animals. Here we explore the function of the pathway in the somatic stem cells of Hydra, a long-lived freshwater cnidarian. Hydra have three stem cell populations, all of which express PIWI proteins; endodermal and ectodermal epithelial stem cells are somatic, whereas the interstitial stem cells have germline competence. To study somatic function of the pathway we isolated piRNAs from Hydra that lack the interstitial lineage and found that these somatic piRNAs map predominantly to TE transcripts and display the conserved sequence signatures typical of germline piRNAs. Three lines of evidence suggest that the PIWI-piRNA pathway represses TEs in Hydra epithelial stem cells. First, epithelial knockdown of the Hydra piwi gene hywi resulted in upregulation of TE expression. Second, degradome sequencing revealed evidence of PIWI-mediated cleavage of TE RNAs in epithelial cells using the ping-pong mechanism. Finally, we demonstrated a direct association between Hywi protein and TE transcripts in epithelial cells using RNA immunoprecipitation. Altogether, our data reveal that the PIWI-piRNA pathway represses TE expression in the somatic cell lineages of Hydra, which we propose contributes to the extreme longevity of the organism. Furthermore, our results, in combination with others, suggest that somatic TE repression is an ancestral function of the PIWI-piRNA pathway.
2019-08-07 | GSE135440 | GEO
Project description:PIWI clade Argonaute proteins and their associated piRNAs are essential guardians of genome integrity, silencing transposable elements through distinct nuclear and cytoplasmic pathways. Nuclear PIWI proteins direct heterochromatin formation to repress transposon transcription, while cytoplasmic PIWIs cleave transposon transcripts to initiate piRNA amplification. Both processes rely on target RNA recognition by PIWI–piRNA complexes, yet how this recognition leads to pathway-specific effector recruitment has remained unclear. Here, we show that target engagement triggers the formation of conserved PIWI* complexes—comprising a PIWI protein, a piRNA–target RNA duplex, a GTSF-family protein, and Maelstrom—that serve as molecular platforms to recruit downstream effectors. In Drosophila, nuclear Piwi* engages the SFiNX complex to induce transcriptional silencing, while cytoplasmic Aubergine* complexes recruit the helicase Spindle-E to promote piRNA biogenesis. Evolutionary analysis reveals that PIWI* complex formation is deeply conserved across metazoans, uncovering an ancient mechanism that couples small RNA-guided target recognition to effector function. These findings define a unifying molecular principle for piRNA-mediated silencing across cellular compartments.
2025-08-11 | PXD066474 | Pride
Project description:Nearly half of the mammalian genome is composed of repeated sequences. In Drosophila, PIWI proteins exert control over transposons. However, mammalian PIWI proteins, Miwi and Mili, partner with piRNAs that are depleted of repeat sequences, raising questions about a role for mammalian PIWIs in transposon control. A search for murine small RNAs that might program PIWI proteins for transposon suppression revealed developmentally regulated piRNA loci, some of which resemble transposon master control loci of Drosophila. We also find evidence of an adaptive amplification loop in which PIWI catalyzes formation of piRNA 5’ ends. Mili mutants de-repress L1 and IAP and lose DNA methylation of L1 elements, demonstrating an evolutionarily conserved role for PIWI proteins in transposon suppression. Keywords: small RNA profile, piRNA
2007-04-20 | GSE7414 | GEO
Project description:Most piRNAs in the Drosophila female germline are transcribed from heterochromatic regions called dual-strand piRNA clusters. Histone 3 lysine 9 trimethylation (H3K9me3) is required for licensing piRNA production by these clusters. However, it is unclear when and how they acquire this permissive heterochromatic state. Although it has been suggested that piRNA cluster licensing is Piwi-independent, here we show that transient Piwi depletion in Drosophila embryos, using a refined knock-down system, results in H3K9me3 decrease at piRNA clusters. This is accompanied by aberrant maturation of piRNA precursor transcripts, accumulation of transposable element transcripts and female sterility. Conversely, Piwi knock-down at later developmental stages does not disturb piRNA cluster licensing, as previously reported. These results indicate that the identity of piRNA clusters is epigenetically acquired in a Piwi-dependent manner during a limited embryonic development window, which is reminiscent of the widespread genome reprogramming occurring during early mammalian zygotic development.
2017-04-27 | GSE83236 | GEO
Project description:Most piRNAs in the Drosophila female germline are transcribed from heterochromatic regions called dual-strand piRNA clusters. Histone 3 lysine 9 trimethylation (H3K9me3) is required for licensing piRNA production by these clusters. However, it is unclear when and how they acquire this permissive heterochromatic state. Although it has been suggested that piRNA cluster licensing is Piwi-independent, here we show that transient Piwi depletion in Drosophila embryos, using a refined knock-down system, results in H3K9me3 decrease at piRNA clusters. This is accompanied by aberrant maturation of piRNA precursor transcripts, accumulation of transposable element transcripts and female sterility. Conversely, Piwi knock-down at later developmental stages does not disturb piRNA cluster licensing, as previously reported. These results indicate that the identity of piRNA clusters is epigenetically acquired in a Piwi-dependent manner during a limited embryonic development window, which is reminiscent of the widespread genome reprogramming occurring during early mammalian zygotic development.
2017-04-27 | GSE83235 | GEO
Project description:Most piRNAs in the Drosophila female germline are transcribed from heterochromatic regions called dual-strand piRNA clusters. Histone 3 lysine 9 trimethylation (H3K9me3) is required for licensing piRNA production by these clusters. However, it is unclear when and how they acquire this permissive heterochromatic state. Although it has been suggested that piRNA cluster licensing is Piwi-independent, here we show that transient Piwi depletion in Drosophila embryos, using a refined knock-down system, results in H3K9me3 decrease at piRNA clusters. This is accompanied by aberrant maturation of piRNA precursor transcripts, accumulation of transposable element transcripts and female sterility. Conversely, Piwi knock-down at later developmental stages does not disturb piRNA cluster licensing, as previously reported. These results indicate that the identity of piRNA clusters is epigenetically acquired in a Piwi-dependent manner during a limited embryonic development window, which is reminiscent of the widespread genome reprogramming occurring during early mammalian zygotic development.
2017-04-27 | GSE83234 | GEO
Project description:Transposable elements (TEs) can damage genomes, thus organisms use a variety of mechanisms to repress TE expression. The PIWI-piRNA pathway is a small RNA pathway that represses TE expression in the germline of animals. Here we explore the function of the pathway in the somatic stem cells of Hydra, a long-lived freshwater cnidarian. Hydra have three stem cell populations, all of which express PIWI proteins; endodermal and ectodermal epithelial stem cells (ESCs) are somatic, whereas the interstitial stem cells have germline competence. To study somatic function of the pathway, we isolated piRNAs from Hydra that lack the interstitial lineage and found that these somatic piRNAs map predominantly to TE transcripts and display the conserved sequence signatures typical of germline piRNAs. Three lines of evidence suggest that the PIWI-piRNA pathway represses TEs in Hydra ESCs. First, epithelial knockdown of the Hydra piwi gene hywi resulted in up-regulation of TE expression. Second, degradome sequencing revealed evidence of PIWI-mediated cleavage of TE RNAs in epithelial cells using the ping-pong mechanism. Finally, we demonstrated a direct association between Hywi protein and TE transcripts in epithelial cells using RNA immunoprecipitation. Altogether, our data reveal that the PIWI-piRNA pathway represses TE expression in the somatic cell lineages of Hydra, which we propose contributes to the extreme longevity of the organism. Furthermore, our results, in combination with others, suggest that somatic TE repression is an ancestral function of the PIWI-piRNA pathway.
| S-EPMC7161359 | biostudies-literature
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:The flamenco (flam) locus is the most prominent piRNA cluster locus expressed in Drosophila ovarian follicle cells that is required for female fertility and silencing of gypsy/mdg4 transposons. Although P-element insertions in the flam promoter region disrupts flam piRNAs and cause female infertility, the flam enhancer architecture is still poorly understood. To illuminate flam’s regulation, we uncovered novel shadow enhancer (SE) sequences within the first exons of flam via promoter-bashing assays in OSS cells. We confirmed the SE relevance in vivo with new Drosophila flam deletion mutants of these regions that compromised flam piRNA expression and lowered female fertility from unleashed transposon expression. In a proteomic analysis of proteins associated with these SE sequences, the MAF transcription factor Traffic jam (Tj) emerged as the most prominent binding candidate. With Tj knockdowns in OSS cells, we see a coordinated loss of flam transcripts and piRNAs as well as a decreased expression of many Piwi pathway genes including piwi, which then also coincided with increased transposon RNA levels. We conducted ChIP-seq of Tj’s interaction at Piwi pathway gene promoters and hundreds of other genes important for follicle cell development. Lastly, we utilized transient Tj knockdown in the fly ovary to support our conclusions of how Tj orchestrates the complex Piwi pathway network in Drosophila follicle cells.
2025-04-01 | PXD052946 | Pride
Project description:In Drosophila, PIWI proteins and bound PIWI interacting RNAs (piRNAs) form the core of a small RNA mediated defense system against selfish genetic elements. Within germline cells piRNAs are processed from piRNA clusters and transposons to be loaded into Piwi/Aubergine/AGO3 and a subset of piRNAs undergoes target dependent amplification. In contrast, gonadal somatic support cells express only Piwi, lack signs of piRNA amplification and exhibit primary piRNA biogenesis from piRNA clusters. Neither piRNA processing/loading nor Piwi mediated target silencing is understood at the genetic, cellular or molecular level. We developed an in vivo RNAi assay for the somatic piRNA pathway and identified the RNA helicase Armitage, the Tudor domain containing RNA helicase Yb and the putative nuclease Zucchini as essential factors for primary piRNA biogenesis. Lack of any of these proteins leads to transposon de-silencing, to a collapse in piRNA levels and to a failure in Piwi nuclear accumulation. We show that Armitage and Yb interact physically and co-localize in cytoplasmic Yb-bodies, which flank P-bodies. Loss of Zucchini leads to an accumulation of Piwi and Armitage in Yb-bodies indicating that Yb-bodies are sites of primary piRNA biogenesis.
2010-10-04 | GSE23560 | GEO