Innate, translation-dependent silencing of an invasive transposon in Arabidopsis
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ABSTRACT:
PROVIDER: PRJNA704712 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13780863.fastq.gz | Fastqsanger.gz | |||
| SRR13780864.fastq.gz | Fastqsanger.gz | |||
| SRR13780865.fastq.gz | Fastqsanger.gz | |||
| SRR13780866.fastq.gz | Fastqsanger.gz | |||
| SRR13780867.fastq.gz | Fastqsanger.gz |
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Project description:Co-evolution between hosts' and parasites' genomes shapes diverse pathways of acquired immunity based on silencing small (s)RNAs. In plants, sRNAs cause heterochromatinization, sequence-degeneration and, ultimately, loss-of-autonomy of most transposable elements (TEs). Recognition of newly-invasive plant TEs, by contrast, involves an innate antiviral-like silencing response. To investigate this response's activation, we studied the single-copy element EVADÉ (EVD), one of few representatives of the large Ty1/Copia family able to proliferate in Arabidopsis when epigenetically-reactivated. In Ty1/Copia-elements, a short subgenomic mRNA (shGAG) provides the necessary excess of structural GAG protein over the catalytic components encoded by the full-length genomic flGAG-POL. We show here that the predominant cytosolic distribution of shGAG strongly favors its translation over mostly-nuclear flGAG-POL. During this process, an unusually intense ribosomal stalling event coincides with mRNA breakage yielding unconventional 5'OH RNA fragments that evade RNA-quality-control. The starting-point of sRNA production by RNA-DEPENDENT-RNA-POLYMERASE-6 (RDR6), exclusively on shGAG, occurs precisely at this breakage point. This hitherto-unrecognized "translation-dependent silencing" (TdS) is independent of codon-usage or GC-content and is not observed on TE remnants populating the Arabidopsis genome, consistent with their poor association, if any, with polysomes. We propose that TdS forms a primal defense against EVD de novo invasions that underlies its associated sRNA pattern.
2021-08-08 | GSE167484 | GEO
Project description:Co-evolution between hosts' and parasites' genomes shapes diverse pathways of acquired immunity based on silencing small (s)RNAs. In plants, sRNAs cause heterochromatinization, sequence degeneration, and, ultimately, loss of autonomy of most transposable elements (TEs). Recognition of newly invasive plant TEs, by contrast, involves an innate antiviral-like silencing response. To investigate this response's activation, we studied the single-copy element EVADÉ (EVD), one of few representatives of the large Ty1/Copia family able to proliferate in Arabidopsis when epigenetically reactivated. In Ty1/Copia elements, a short subgenomic mRNA (shGAG) provides the necessary excess of structural GAG protein over the catalytic components encoded by the full-length genomic flGAG-POL. We show here that the predominant cytosolic distribution of shGAG strongly favors its translation over mostly nuclear flGAG-POL. During this process, an unusually intense ribosomal stalling event coincides with mRNA breakage yielding unconventional 5'OH RNA fragments that evade RNA quality control. The starting point of sRNA production by RNA-DEPENDENT-RNA-POLYMERASE-6 (RDR6), exclusively on shGAG, occurs precisely at this breakage point. This hitherto-unrecognized "translation-dependent silencing" (TdS) is independent of codon usage or GC content and is not observed on TE remnants populating the Arabidopsis genome, consistent with their poor association, if any, with polysomes. We propose that TdS forms a primal defense against EVD de novo invasions that underlies its associated sRNA pattern.
| S-EPMC8892269 | biostudies-literature
Project description:Co-evolution between hosts' and parasites' genomes shapes diverse pathways of acquired immunity based on silencing small (s)RNAs. In plants, sRNAs cause heterochromatinization, sequence-degeneration and, ultimately, loss-of-autonomy of most transposable elements (TEs). Recognition of newly-invasive plant TEs, by contrast, involves an innate antiviral-like silencing response. To investigate this response's activation, we studied the single-copy element EVADÉ (EVD), one of few representatives of the large Ty1/Copia family able to proliferate in Arabidopsis when epigenetically-reactivated. In Ty1/Copia-elements, a short subgenomic mRNA (shGAG) provides the necessary excess of structural GAG protein over the catalytic components encoded by the full-length genomic flGAG-POL. We show here that the predominant cytosolic distribution of shGAG strongly favors its translation over mostly-nuclear flGAG-POL. During this process, an unusually intense ribosomal stalling event coincides with mRNA breakage yielding unconventional 5'OH RNA fragments that evade RNA-quality-control. The starting-point of sRNA production by RNA-DEPENDENT-RNA-POLYMERASE-6 (RDR6), exclusively on shGAG, occurs precisely at this breakage point. This hitherto-unrecognized "translation-dependent silencing" (TdS) is independent of codon-usage or GC-content and is not observed on TE remnants populating the Arabidopsis genome, consistent with their poor association, if any, with polysomes. We propose that TdS forms a primal defense against EVD de novo invasions that underlies its associated sRNA pattern.
| S-SCDT-EMBOR-2021-53400-T | biostudies-other
Project description:In animal gonads, the PIWI-interacting RNA (piRNA) pathway guards genome integrity in part through the co-transcriptional gene silencing of transposon insertions. In Drosophila ovaries, piRNA-loaded Piwi detects nascent transposon transcripts and instructs heterochromatin formation through the Panoramix-induced co-transcriptional silencing (PICTS) complex, containing Panoramix, Nxf2 and Nxt1. Here, we report that the highly conserved dynein light chain LC8/Cut-up (Ctp) is an essential component of the PICTS complex. Loss of Ctp results in transposon de-repression and a reduction in repressive chromatin marks specifically at transposon loci. In turn, Ctp can enforce transcriptional silencing when artificially recruited to RNA and DNA reporters. We show that Ctp drives dimerisation of the PICTS complex through its interaction with conserved motifs within Panoramix. Artificial dimerisation of Panoramix bypasses the necessity for its interaction with Ctp, demonstrating that conscription of a protein from a ubiquitous cellular machinery has fulfilled a fundamental requirement for a transposon silencing complex.
2021-01-26 | PXD022105 | Pride
Project description:In animal gonads, the PIWI-interacting RNA (piRNA) pathway guards genome integrity in part through the co-transcriptional gene silencing of transposon insertions. In Drosophila ovaries, piRNA-loaded Piwi detects nascent transposon transcripts and instructs heterochromatin formation through the Panoramix-induced co-transcriptional silencing (PICTS) complex, containing Panoramix, Nxf2 and Nxt1. Here, we report that the highly conserved dynein light chain LC8/Cut-up (Ctp) is an essential component of the PICTS complex. Loss of Ctp results in transposon de-repression and a reduction in repressive chromatin marks specifically at transposon loci. In turn, Ctp can enforce transcriptional silencing when artificially recruited to RNA and DNA reporters. We show that Ctp drives dimerisation of the PICTS complex through its interaction with conserved motifs within Panoramix. Artificial dimerisation of Panoramix bypasses the necessity for its interaction with Ctp, demonstrating that conscription of a protein from a ubiquitous cellular machinery has fulfilled a fundamental requirement for a transposon silencing complex.
2021-01-26 | PXD022103 | Pride
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:This SuperSeries is composed of the following subset Series: GSE32180: MIWI catalysis is required for piRNA amplification-independent LINE1 transposon silencing [microarray] GSE32184: MIWI catalysis is required for piRNA amplification-independent LINE1 transposon silencing [deep sequencing] Refer to individual Series
2011-11-30 | E-GEOD-32183 | biostudies-arrayexpress
Project description:The repression of transposons by the Piwi-interacting RNA (piRNA) pathway is essential to protect animal germ cells. In Drosophila ovaries, Panoramix (Panx) enforces transcriptional silencing by binding to the target-engaged Piwi-piRNA complex, although the precise mechanisms by which this occurs remain elusive. Here, we show that Panx functions together with a germline specific paralogue of a nuclear export factor, dNxf2, and its cofactor dNxt1 (p15), as a ternary complex to suppress transposon expression. Similar to Panx, dNxf2 is essential for animal fertility. Structural and functional analyses demonstrate that dNxf2 binds Panx via its UBA domain, which plays an important role in transposon silencing. Unexpectedly, dNxf2 interacts directly with dNxf1 (TAP), a general nuclear export factor. As a result, dNxf2 prevents dNxf1 from binding to the FG repeats of the nuclear pore complex, a process required for proper RNA export. Transient tethering of dNxf2 to nascent transcripts leads to their nuclear retention. Thus, dNxf2 functions in a Pandas (Panoramix dNxf2 dependent TAP/p15 silencing) complex, which counteracts the canonical RNA exporting machinery and restricts transposons to the nuclear peripheries. Our findings may have broader implications for understanding how RNA metabolism regulates epigenetic gene silencing and heterochromatin formation.
2019-08-06 | PXD014926 |
Project description:The repression of transposons by the Piwi-interacting RNA (piRNA) pathway is essential to protect animal germ cells. In Drosophila ovaries, Panoramix (Panx) enforces transcriptional silencing by binding to the target-engaged Piwi-piRNA complex, although the precise mechanisms by which this occur remain elusive. Here, we show that Panx functions together with a germline specific paralogue of a nuclear export factor, dNxf2, and its cofactor dNxt1 (p15) as a ternary complex to suppress transposon expression. Structural and functional analysis demonstrate that dNxf2 binds Panx via its UBA domain and play an important role in transposon silencing through binding to transposon transcripts directly. Unexpectedly, dNxf2 interacts directly with dNxf1 (TAP), which is also essential for transposon silencing. Transient tethering of dNxf2 to nascent transcripts leads to their nuclear retention. Therefore, we propose that dNxf2 may function as a Pandas (Panoramix dNxf2 dependent TAP/p15 silencing) complex, which counteracts the canonical RNA exporting machinery (TAP/p15) and restricts transposons to nuclear peripheries. Our finding may have broader implications for understanding how RNA metabolism modulates epigenetic gene silencing and heterochromatin formation.
2019-08-09 | GSE130041 | GEO
Project description:The repression of transposons by the Piwi-interacting RNA (piRNA) pathway is essential to protect animal germ cells. In Drosophila ovaries, Panoramix (Panx) enforces transcriptional silencing by binding to the target-engaged Piwi-piRNA complex, although the precise mechanisms by which this occur remain elusive. Here, we show that Panx functions together with a germline specific paralogue of a nuclear export factor, dNxf2, and its cofactor dNxt1 (p15) as a ternary complex to suppress transposon expression. Structural and functional analysis demonstrate that dNxf2 binds Panx via its UBA domain and play an important role in transposon silencing through binding to transposon transcripts directly. Unexpectedly, dNxf2 interacts directly with dNxf1 (TAP), which is also essential for transposon silencing. Transient tethering of dNxf2 to nascent transcripts leads to their nuclear retention. Therefore, we propose that dNxf2 may function as a Pandas (Panoramix dNxf2 dependent TAP/p15 silencing) complex, which counteracts the canonical RNA exporting machinery (TAP/p15) and restricts transposons to nuclear peripheries. Our finding may have broader implications for understanding how RNA metabolism modulates epigenetic gene silencing and heterochromatin formation.
2019-08-09 | GSE121158 | GEO