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RNAi-dependent Polycomb repression controls transposable elements in Tetrahymena

ABSTRACT: RNAi-dependent Polycomb repression controls transposable elements in Tetrahymena

PROVIDER: PRJNA484827 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7651370.fastq.gz	Fastqsanger.gz
	SRR7651380.fastq.gz	Fastqsanger.gz
	SRR7651390.fastq.gz	Fastqsanger.gz
	SRR7651400_1.fastq.gz	Fastqsanger.gz
	SRR7651400_2.fastq.gz	Fastqsanger.gz

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RNAi-dependent Polycomb repression controls transposable elements in Tetrahymena [RNA-seq]

Project description:RNA interference (RNAi) and Polycomb repression play evolutionarily conserved and often coordinated roles in transcriptional silencing. Here we show that in the protozoan Tetrahymena thermophila, germ line-specific internally eliminated sequences (IES) - many related to transposable elements (TE) - are transcriptionally activated in mutants deficient in the RNAi-dependent Polycomb repression pathway. Mobilization of recently duplicated TE also dramatically increases in these mutants. Importantly, transcriptional silencing and activation of TE-related sequences are accompanied by switching between noncoding RNA (ncRNA) and mRNA production, which can be affected by co-transcriptional processing as well as RNAi and Polycomb repression. We posit that interplay between RNAi and Polycomb repression is a widespread phenomenon, whose ancestral role is epigenetic silencing of TE.

2019-03-01 | GSE118199 | GEO

RNAi-dependent Polycomb repression controls transposable elements in Tetrahymena [small RNA-seq]

Project description:RNA interference (RNAi) and Polycomb repression play evolutionarily conserved and often coordinated roles in transcriptional silencing. Here we show that in the protozoan Tetrahymena thermophila, germ line-specific internally eliminated sequences (IES)—many related to transposable elements (TE)—are transcriptionally activated in mutants deficient in the RNAi-dependent Polycomb repression pathway. Mobilization of recently duplicated TE also dramatically increases in these mutants. Importantly, transcriptional silencing and activation of TE-related sequences are accompanied by switching between noncoding RNA (ncRNA) and mRNA production, which can be affected by co-transcriptional processing as well as RNAi and Polycomb repression. We posit that interplay between RNAi and Polycomb repression is a widespread phenomenon, whose ancestral role is epigenetic silencing of TE.

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RNAi-dependent Polycomb repression controls transposable elements in Tetrahymena [RNA-seq]

Project description:RNAi-dependent Polycomb repression controls transposable elements in Tetrahymena [RNA-seq]

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RNAi-dependent Polycomb repression controls transposable elements in Tetrahymena [small RNA-seq]

Project description:RNAi-dependent Polycomb repression controls transposable elements in Tetrahymena [small RNA-seq]

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RNAi-dependent <i>Polycomb</i> repression controls transposable elements in <i>Tetrahymena</i>.

Project description:RNAi and Polycomb repression play evolutionarily conserved and often coordinated roles in transcriptional silencing. Here, we show that, in the protozoan Tetrahymena thermophila, germline-specific internally eliminated sequences (IESs)-many related to transposable elements (TEs)-become transcriptionally activated in mutants deficient in the RNAi-dependent Polycomb repression pathway. Germline TE mobilization also dramatically increases in these mutants. The transition from noncoding RNA (ncRNA) to mRNA production accompanies transcriptional activation of TE-related sequences and vice versa for transcriptional silencing. The balance between ncRNA and mRNA production is potentially affected by cotranscriptional processing as well as RNAi and Polycomb repression. We posit that interplay between RNAi and Polycomb repression is a widely conserved phenomenon, whose ancestral role is epigenetic silencing of TEs.

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RNAi-dependent Polycomb repression controls transposable elements in Tetrahymena

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-02-28 | GSE118200 | GEO

An RNAi-dependent Polycomb Repression Pathway Is Required for Co-transcriptional Silencing of Transposable Elements

Project description:An RNAi-dependent Polycomb Repression Pathway Is Required for Co-transcriptional Silencing of Transposable Elements

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Paramecium Polycomb Repressive Complex 2 physically interacts with the small RNA binding PIWI protein to repress transposable elements

Project description:Polycomb Repressive Complex 2 (PRC2) maintains transcriptionally silent genes in a repressed state via deposition of histone H3 K27 trimethyl (me3) marks. PRC2 has also been implicated in silencing transposable elements (TEs) yet how PRC2 is targeted to TEs remains unclear. To address this question, we performed tandem affinity purification combined with mass spectrometry and identified proteins that physically interact with the Paramecium Enhancer-of-zeste Ezl1 enzyme, which catalyzes H3K9me3 and H3K27me3 deposition at TEs. We show that the Paramecium PRC2 core complex comprises four subunits, each required in vivo for catalytic activity. We also identify PRC2 cofactors, including the RNA interference (RNAi) effector Ptiwi09, which are necessary to target H3K9me3 and H3K27me3 to TEs. We find that the physical interaction between PRC2 and the RNAi pathway is mediated by a RING finger protein and that small RNA recruitment of PRC2 to TEs is analogous to the small RNA recruitment of H3K9 methylation SU(VAR)3-9 enzymes.

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An RNAi-dependent Polycomb Repression Pathway Is Required for Co-transcriptional Silencing of Transposable Elements

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Project description:The Polycomb system modifies chromatin and plays an essential role in repressing gene expression to control normal mammalian development. However, the components and mechanisms that define how Polycomb protein complexes achieve this remain enigmatic. Here we use combinatorial genetic perturbation coupled with quantitative genomics to discover the central determinants of Polycomb-mediated gene repression in mouse embryonic stem cells. We demonstrate that canonical Polycomb repressive complex 1 (PRC1), which mediates higher order chromatin structures, contributes little to gene repression. Instead, we uncover an unexpectedly high degree of synergy between variant PRC1 complexes which is fundamental to gene repression. We further demonstrate that variant PRC1 complexes are responsible for distinct pools of H2A monoubiquitylation that are associated with repression of Polycomb target genes and silencing during X-chromosome inactivation. Together, these discoveries reveal a new variant PRC1-dependent logic for Polycomb-mediated gene repression.

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