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Role of PML in repression of transposable elements and in embryonic stem cell fate

ABSTRACT: Role of PML in repression of transposable elements and in embryonic stem cell fate

PROVIDER: PRJEB44045 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR5638893.fastq.gz	Fastqsanger.gz
	ERR5638894.fastq.gz	Fastqsanger.gz
	ERR5638895.fastq.gz	Fastqsanger.gz
	ERR5638896.fastq.gz	Fastqsanger.gz
	ERR5638897.fastq.gz	Fastqsanger.gz

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Role of PML in repression of transposable elements and in embryonic stem cell fate

Project description:RNA-seq analysis from 2 Pml-/- and 3 Pml+/+ mESC samples

2022-02-01 | E-MTAB-10153 | biostudies-arrayexpress

Role of PML in repression of transposable elements and in embryonic stem cell fate

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Unbiased in vivo exploration of nuclear bodies-enhanced sumoylation reveals that PML orchestrates embryonic stem cell fate

Project description:Membrane-less organelles are condensates formed by phase separation whose functions often remain enigmatic. Upon oxidative stress, PML scaffolds Nuclear Bodies (NBs) to regulate senescence or metabolic adaptation, but their role in pluripotency remains elusive. Here we establish that PML is required for basal SUMO2/3 conjugation in mESCs and oxidative stress-driven sumoylation in mESCs or in vivo. PML NBs create an oxidationprotective environment for UBC9-driven SUMO2/3 conjugation of PML partners, often followed by their poly-ubiquitination and degradation. Differential in vivo proteomics identified several members of the KAP1 complex as PML NB-dependent SUMO2-targets. The latter drives functional activation of this key epigenetic repressor. Accordingly, Pml-/- mESCs reexpress transposable elements and display features of totipotent-like cells, a process further enforced by PML-controlled SUMO2-conjugation of DPPA2. Finally, PML is required for adaptive stress responses in mESCs. Collectively, PML orchestrates mESC fate through SUMO2-conjugation of key transcriptional or epigenetic regulators, raising new mechanistic hypotheses about PML roles in normal or cancer stem cells.

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Unbiased in vivo exploration of nuclear bodies-enhanced sumoylation reveals that PML orchestrates embryonic stem cell fate (II)

2023-03-06 | PXD032240 | Pride

RNAi-dependent Polycomb repression controls transposable elements in Tetrahymena

Project description:RNAi-dependent Polycomb repression controls transposable elements in Tetrahymena

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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 [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 [small RNA-seq]

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

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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.

2019-03-01 | GSE118198 | GEO

Transposable elements are co-opted as oncogenic regulatory elements by lineage-specific transcription factors in prostate cancer

Project description:Transposable elements hold regulatory functions to impact cell fate determination by controlling gene expression, which when altered can promote oncogenesis. Despite accounting for half of the human genome, little is known about the transcriptional mechanisms that confer regulatory properties to transposable elements in pluripotent, mature versus oncogenic cell states. Through positional analysis over repetitive DNA sequence of H3K27ac ChIP-seq from 32 different normal cell and tissue states, we report pluripotent stem and mature cell states-specific “regulatory transposable elements”. Those specific to pluripotent stem cells are binding sites for the pluripotency factors NANOG, SOX2 and OCT4. In mature cell and tissue states, regulatory transposable elements are docking sites for lineage-specific transcription factors, such as AR and FOXA1 in benign prostate epithelium. Expanding the positional analysis to localized prostate tumors, we show how cancer cell states remaining dependent on AR share regulatory transposable elements with pluripotent stem cells. These include regulatory transposable elements, such as Tigger3a, that serve as binding sites for AR and whose regulatory functions are required for prostate cancer cell growth. Together, our results suggest that oncogenesis differs from normal cell fate determination by hijacking pluripotent stem cells regulatory transposable elements that serve as docking sites for lineage-specific transcription factors.

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