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.
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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: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 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
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 | GSE130042 | GEO
Project description:RNA-directed transposon silencing operates in the mammalian soma and germline tosafeguard genomic integrity. The piRNA pathway and the HUSHcomplex identify activetransposons through recognition of their nascent transcripts, but mechanisticunderstanding of how these distinct pathways evolved is lacking. TASOR is anessential component of the HUSH complex. TASOR’s DUF3715 domain adopts apseudo-PARP structure and is required for transposon silencing in a mannerindependent of complex assembly. TEX15, an essential piRNA pathway factor, alsocontains the DUF3715 domain. Here, we show that TASOR’s and TEX15’s DUF3715domain share extensive structural homology. We found that the DUF3715 domain arosein early eukaryotes and that in vertebrates it is restricted to TEX15, TASOR, andTASORB orthologues. While TASOR-like proteins are found throughout metazoa,TEX15 is vertebrate specific. The branchingof TEX15 and TASOR-like DUF3715 domainlikely occurred in early metazoan evolution. Remarkably, despite this vast evolutionarydistance, the DUF3715 domain from divergent TEX15 sequences can functionallysubstitute for the same domain in TASOR and mediates transposon silencing. We havethus termed this domain of unknown function as the RNA-directed pseudo-PARPtransposon silencing (RDTS) domain. In summary, we show an unexpected functionallink between these critical transposon silencing pathways.
2023-10-26 | GSE234730 | GEO