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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Piwi modulates chromatin accessibility by regulating multiple factors including histone H1 to repress transposons

ABSTRACT: PIWI-interacting RNAs (piRNAs) mediate transposable element (TE) silencing at the transcriptional or post-transcriptional level in animal gonads. In the Drosophila ovary, Piwiâ??piRNA complexes (Piwiâ??piRISCs) repress TE transcription by modifying the chromatin state, such as H3K9me3 marks. Here, we demonstrate that Piwi physically interacts with linker histone H1. Depletion of Piwi decreases H1 density on target loci, leading to TE derepression. Loss of H1 results in gain of chromatin accessibility at target loci without affecting H3K9me3 and heterochromatin protein 1a (HP1a) density at the same loci. Piwi-mediated TE silencing also requires HP1a by regulating chromatin accessibility through its association with target loci. Thus, Piwiâ??piRISCs require both H1 and HP1a to repress TEs, and the silencing is correlated with the state of chromatin formation rather than H3K9me3 marks. These findings suggest that Piwiâ??piRISCs regulate the interaction of chromatin components with target loci to maintain silencing of the TE state through the modulation of chromatin accessibility. RNA levels, H1 and H3K9me3 occupancy, chromatin accessibility, and Piwi-associated small RNA levels in ovarian somatic cells (OSC) depleted of piRNA pathway components and H1.

ORGANISM(S): Drosophila melanogaster

SUBMITTER: Haruhiko Siomi

PROVIDER: E-GEOD-81434 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Piwi modulates chromatin accessibility by regulating multiple factors including histone H1 to repress transposons

Project description:PIWI-interacting RNAs (piRNAs) mediate transposable element (TE) silencing at the transcriptional or post-transcriptional level in animal gonads. In the Drosophila ovary, Piwi–piRNA complexes (Piwi–piRISCs) repress TE transcription by modifying the chromatin state, such as H3K9me3 marks. Here, we demonstrate that Piwi physically interacts with linker histone H1. Depletion of Piwi decreases H1 density on target loci, leading to TE derepression. Loss of H1 results in gain of chromatin accessibility at target loci without affecting H3K9me3 and heterochromatin protein 1a (HP1a) density at the same loci. Piwi-mediated TE silencing also requires HP1a by regulating chromatin accessibility through its association with target loci. Thus, Piwi–piRISCs require both H1 and HP1a to repress TEs, and the silencing is correlated with the state of chromatin formation rather than H3K9me3 marks. These findings suggest that Piwi–piRISCs regulate the interaction of chromatin components with target loci to maintain silencing of the TE state through the modulation of chromatin accessibility.

2016-06-30 | GSE81434 | GEO

Complex Genetic Interactions between Piwi and HP1a in the Repression of Transposable Elements and Tissue-Specific Genes in the Ovarian Germline

Project description:Insertions of transposable elements (TEs) in eukaryotic genomes are usually associated with repressive chromatin, which spreads to neighbouring genomic sequences. In ovaries of Drosophila melanogaster, the Piwi-piRNA pathway plays a key role in the transcriptional silencing of TEs considered to be exerted mostly through the establishment of H3K9me3 histone marks recruiting Heterochromatin Protein 1a (HP1a). Here, using RNA-seq, we investigated the expression of TEs and the adjacent genomic regions upon Piwi and HP1a germline knockdowns sharing a similar genetic background. We found that the depletion of Piwi and HP1a led to the derepression of only partially overlapping TE sets. Several TEs were silenced predominantly by HP1a, whereas the upregulation of some other TEs was more pronounced upon Piwi knockdown and, surprisingly, was diminished upon a Piwi/HP1a double-knockdown. We revealed that HP1a loss influenced the expression of thousands of protein-coding genes mostly not adjacent to TE insertions and, in particular, downregulated a putative transcriptional factor required for TE activation. Nevertheless, our results indicate that Piwi and HP1a cooperatively exert repressive effects on the transcription of euchromatic loci flanking the insertions of some Piwi-regulated TEs. We suggest that this mechanism controls the silencing of a small set of TE-adjacent tissue-specific genes, preventing their inappropriate expression in ovaries.

2021-12-22 | GSE186867 | GEO

The Mi-2 nucleosome remodeler and the Rpd3 histone deacetylase are involved in piRNA-guided heterochromatin formation

Project description:In eukaryotes, trimethylation of lysine 9 on histone H3 (H3K9) is associated with transcriptional silencing of transposable elements (TEs). In drosophila ovaries, this heterochromatic repressive mark is thought to be deposited by SetDB1 on TE genomic loci after the initial recognition of nascent transcripts by PIWI-interacting RNAs (piRNAs) loaded on the Piwi protein. Here, we show that the nucleosome remodeler Mi-2, in complex with its partner MEP-1, forms a subunit that is transiently associated, in a MEP-1 C-terminus-dependent manner, with known Piwi interactors, including a recently reported SUMO ligase Su(var)2-10. Together with the histone deacetylase Rpd3, this module is involved in the piRNA-dependent TE silencing, correlated with H3K9 deacetylation and trimethylation. Therefore. drosophila piRNA-mediated transcriptional silencing involves three epigenetic effectors, a remodeler, Mi-2, an eraser, Rpd3 and a writer, SetDB1, in addition to the Su(var)2-10 SUMO ligase.

2020-07-21 | PXD018749 | Pride

Transcriptional silencing of transposable elements by Piwi and its impact on chromatin and gene expression

Project description:Eukaryotic genomes are colonized by transposable elements whose uncontrolled activity results in genomic instability. The piRNA pathway silences transposons in animal gonads, yet how this is achieved molecularly remains controversial. We assign an essential role to the HMG protein Maelstrom in the process of Piwi mediated silencing in Drosophila. Genome wide assays revealed highly correlated changes in RNA Polymerase II recruitment, nascent RNA output and steady state RNA levels of transposons upon loss of Piwi or Maelstrom. Our data demonstrate piRNA-mediated trans- silencing of hundreds of transposon copies at the transcriptional level. We show that Piwi is required for establishing heterochromatic H3K9me3 marks on transposons and their genomic surrounding. In contrast, loss of Maelstrom impacts transposon H3K9me3 patterns only marginally yet leads to increased heterochromatin spreading, suggesting that Maelstrom acts downstream of or in parallel to H3K9me3. Our work uncovers the widespread influence of transposons and the piRNA pathway on chromatin patterns and gene expression programs. RNA Polymerase II and H3K9me3 occupancy, and steady-state and nascent RNA levels in wild-type ovarian somatic cells (OSC) and RNAi knock-downs of the piRNA pathway components. RNA Polymerase II occupancy in tissue-specific knockdowns of tejas (control) and armi in somatic cells of Drosophila ovary.

2012-11-26 | E-GEOD-41729 | biostudies-arrayexpress

Expression profile and RNA Polymerase II occupancy of transposable elements among knock down of the piRNA pathway components in OSCs

Project description:The PiwiM-bM-^@M-^SpiRNA complex (PiwiM-bM-^@M-^SpiRISC) in Drosophila ovarian somatic cells represses transposons transcriptionally to maintain genome integrity; however, the underlying mechanisms remain obscure. We performed mRNA-seq analysis from OSCs transfected with siRNAs against CG3893, the known piRNA pathway genes, Piwi, Maelstrom, HP1a and Armitage, and the control (EGFP), and PolII ChIP-seqanalysis from OSCs transfected with siRNAs against CG3893, Piwi, Mael and the control (EGFP). This result indicates that CG3893 is a novel factor for primary piRNA pathway in OSCs. RNA levels in wild-type (EGFP control knock-down) ovarian somatic cells (OSC) and RNAi knock-downs of Piwi, Armi, Mael, CG3893, and HP1a. RNA Polymerase II occupancy in wild-type (EGFP control knock-down) ovarian somatic cells (OSC) and RNAi knock-downs of Piwi, Mael, and CG3893.

2013-08-01 | E-GEOD-47006 | biostudies-arrayexpress

Nuclear RNA export factor variant initiates piRNA-guided co-transcriptional silencing

Project description:PIWI-interacting RNAs (piRNAs) are germline-specific small RNAs that form effector complexes with PIWI proteins (Piwi–piRISC complexes) to preserve genomic integrity by repressing transposable elements (TEs). Among PIWI-clade proteins in Drosophila, Piwi transcriptionally silences its targets via heterochromatin formation characterised by H3K9me3 marks and the linker histone H1. Recent studies have shown that Panoramix (Panx) interacts with Piwi–piRISC complexes to induce transcriptional repression of targets mediated by the recruitment of H3K9me3 marks. Here, we identified Nxf2, a nuclear RNA export factor (NXF) variant, as a protein that forms a complex with Panx and Piwi. Nxf2 further associates with p15 (Nxt1), a co-adaptor for nuclear RNA export. However, unlike Nxf1 that plays a major role in mRNA export, Nxf2–p15 instead transcriptionally regulates TEs in the Piwi–piRNA pathway. Panx–Nxf2–p15 complex formation is necessary in the silencing by stabilizing protein levels of Nxf2 and Panx. Notably, ectopic targeting of Nxf2 initiates co-transcriptional repression of the target reporter in a manner independent of H3K9me3 marks or H1. However, continuous silencing requires HP1a and H1. The amino-terminal domain of Nxf2 harbouring RNA binding activity is essential for recruitment of the Piwi–piRISC complex to target TEs. Indeed, Nxf2 directly interacts with target TE transcripts in a Piwi-dependent manner. These findings suggest a model in which the Nxf2–Panx–p15 complex enforces the association of Piwi with target transcripts to trigger co-transcriptional repression, prior to heterochromatin formation in the nuclear piRNA pathway. Our results provide an unexpected connection between an NXF variant and small RNA-mediated co-transcriptional silencing.

2019-07-09 | GSE131950 | GEO

Piwi–piRNA complexes induce stepwise changes in nuclear architecture at target loci

Project description:PIWI-interacting RNAs (piRNAs) are germline-specific small RNAs that form effector complexes with PIWI proteins (Piwi–piRNA complexes), and plays a critical role for preserving genomic integrity by repressing transposable elements (TEs). Drosophila Piwi transcriptionally silences specific targets through heterochromatin formation, and increases H3K9me3 and histone H1. Additionally, Nxf2, a nuclear RNA export factor variant, has been identified as a co-factor. Using ChEP and DamID-seq, we uncover Piwi/Nxf2-dependent target association with nuclear lamins. Hi-C analysis of Piwi or Nxf2 depleted cells reveals decreased intra-TAD and increased inter-TAD interaction in regions harboring Piwi–piRNA target TEs. Using a forced tethering system, we analyze the functional effects of Piwi–piRNA/Nxf2-mediated recruitment of piRNA target regions to the nuclear periphery. Removal of active histone marks is followed by transcriptional silencing, chromatin conformational changes, and H3K9me3 and H1 association. Our data show that the Piwi–piRNA pathway can induce stepwise changes in nuclear architecture and chromatin state at target loci for transcriptional silencing.

2021-07-01 | GSE158082 | GEO

Drosophila Gtsf1 is an essential component of the Piwi mediated transcriptional silencing complex

Project description:The PIWI interacting RNA pathway is a small RNA silencing system that keeps selfish genetic elements such as transposons under control in animal gonads. Several lines of evidence indicate that nuclear PIWI family proteins guide transcriptional silencing of their targets, yet the composition of the underlying silencing complex is unknown. Here we demonstrate that the double CHHC zinc finger protein Gtsf1 is an essential factor for Piwi mediated transcriptional repression in Drosophila. Cells lacking Gtsf1 contain nuclear Piwi loaded with piRNAs, yet Piwi's silencing capacity is ablated. Gtsf1 interacts stably with a sub-population of nuclear Piwi and loss of Gtsf1 phenocopies loss of Piwi in terms of deregulation of transposons, loss of H3K9me3 marks at euchromatic transposon insertions and deregulation of genes in proximity to repressed transposons. We propose that only a small fraction of nuclear Piwi interacts productively with a target RNA, resulting in assembly of a silencing complex with Gtsf1 as one core component. impact of loss of DmGtsf1 on transcription and H3K9m3 in ovarian somatic cells (OSC)

2013-09-06 | E-GEOD-48317 | biostudies-arrayexpress

Impact of nuclear Piwi elimination on chromatin state in Drosophila melanogaster ovaries

Project description:The piRNA-interacting Piwi protein is involved in transcriptional silencing of transposable elements in ovaries of D. melanogaster. Here we characterized the genome-wide effect of nuclear Piwi elimination on the presence of the heterochromatic H3K9me3 mark and HP1a, as well as on the transcription-associated mark H3K4me2. Our results demonstrate that a significant increase in the H3K4me2 level upon nuclear Piwi loss is not accompanied by the alterations in H3K9me3 and HP1a levels for several germline-expressed transposons, suggesting that in this case Piwi prevents transcription by a mechanism distinct from H3K9 methylation. We found that the targets of Piwi-dependent chromatin repression are mainly related to the elements that display a higher level of H3K4me2 modification in the absence of silencing, i.e. most actively transcribed elements. We also show that Piwi-guided silencing does not significantly influence the chromatin state of dual-strand piRNA-producing clusters. In addition, host protein-coding gene expression is essentially not affected due to the nuclear Piwi elimination, but we noted an increase in small nuclear spliceosomal RNAs abundance and propose Piwi involvement in their posttranscriptional regulation. Our work reveals new aspects of transposon silencing in Drosophila, indicating that transcription of transposons can underpin their Piwi dependent silencing, while canonical heterochromatin marks are not obligatory for their repression. Examination of histone modifications in ovaries from two different fly lines- piwiNt/piwi2 (mutant) and piwi/+ (wildtype)

2014-05-19 | E-GEOD-56347 | biostudies-arrayexpress

Impact of nuclear Piwi elimination on chromatin state in Drosophila melanogaster ovaries

2014-05-19 | GSE56347 | GEO

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