Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA329256 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3925060.fastq.gz | Fastqsanger.gz | |||
| SRR3925061.fastq.gz | Fastqsanger.gz | |||
| SRR3925056.fastq.gz | Fastqsanger.gz | |||
| SRR3925057.fastq.gz | Fastqsanger.gz | |||
| SRR3925058.fastq.gz | Fastqsanger.gz |
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Project description:TET-dependent regulation of retrotransposable elements in mouse embryonic stem cells [RNA-seq]
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Project description:TET-dependent regulation of retrotransposable elements in mouse embryonic stem cells
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Project description:TET enzymes oxidise DNA methylation as part of an active demethylation pathway. Despite extensive research into the role of TETs in genome regulation, little is known about their effect on transposable elements (TEs), which make up nearly half of the mouse and human genomes. Epigenetic mechanisms controlling TEs have the potential to affect their mobility and to drive the co-adoption of TEs for the benefit of the host. We have performed a detailed investigation of the role of TET enzymes in the regulation of TEs in mouse embryonic stem cells (ESCs). We found that TET1 and TET2 bind multiple TE classes that harbour a variety of epigenetic signatures indicative of different functional roles. Namely, TETs co-bind with pluripotency factors to enhancer-like TEs that interact with highly expressed genes in ESCs, whose expression is partly maintained by the demethylating action of TET2. TETs and 5-hydroxymethylcytosine are also strongly enriched at the 5’ UTR of full-length, evolutionarily young LINE1 elements, a pattern that is conserved in human embryonic stem cells. TET depletion leads to a marked increase in DNA methylation levels at LINE1s, but surprisingly their expression is stably maintained through additional TET-dependent activities. Specifically, we find that TET1 recruits the SIN3A co-repressive complex to LINE1s, ensuring their repression upon TET-driven hypomethylation. This dual nature of TET action may reflect the evolutionary battle between TEs and the host. Our data implicate TET enzymes in the evolutionary dynamics of TEs, both in the context of exaptation processes and of retrotransposition control.
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Project description:TET enzymes oxidise DNA methylation as part of an active demethylation pathway. Despite extensive research into the role of TETs in genome regulation, little is known about their effect on transposable elements (TEs), which make up nearly half of the mouse and human genomes. Epigenetic mechanisms controlling TEs have the potential to affect their mobility and to drive the co-adoption of TEs for the benefit of the host. We have performed a detailed investigation of the role of TET enzymes in the regulation of TEs in mouse embryonic stem cells (ESCs). We found that TET1 and TET2 bind multiple TE classes that harbour a variety of epigenetic signatures indicative of different functional roles. Namely, TETs co-bind with pluripotency factors to enhancer-like TEs that interact with highly expressed genes in ESCs, whose expression is partly maintained by the demethylating action of TET2. TETs and 5-hydroxymethylcytosine are also strongly enriched at the 5’ UTR of full-length, evolutionarily young LINE1 elements, a pattern that is conserved in human embryonic stem cells. TET depletion leads to a marked increase in DNA methylation levels at LINE1s, but surprisingly their expression is stably maintained through additional TET-dependent activities. Specifically, we find that TET1 recruits the SIN3A co-repressive complex to LINE1s, ensuring their repression upon TET-driven hypomethylation. This dual nature of TET action may reflect the evolutionary battle between TEs and the host. Our data implicate TET enzymes in the evolutionary dynamics of TEs, both in the context of exaptation processes and of retrotransposition control.
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Project description:Dormancy is an essential biological process for the propagation of many life forms through generations and stressful conditions. Early embryos of many mammals are preservable for weeks to months within the uterus under dormancy, which can be induced in vitro through mTOR inhibition. Dormancy features silencing of the genome and abundant heterochromatin formation, which conflicts with the permissive and uncommitted genomic profile of pluripotent cells. Cellular strategies to maintain pluripotency in the fate of this conflict are not known. Here we probed chromatin regulation during embryonic stem cells’ (ESC) entry into dormancy to identify mechanisms that ensure faithful propagation of cellular identity through dormancy. We show a global increase in DNA methylation and loss of chromatin accessibility in dormant ESCs and find that TET DNA demethylases are essential to counteract this trend at key pluripotency regulatory elements, particularly at young LINE1 repeats and active enhancers. Demethylation of these targets by TETs is essential for transcription factor (TF) recruitment and transient chromatin decondensation before hypercompaction. We propose that key regulatory elements are bookmarked coordinately by TETs and TFs in dormancy for maintenance of cellular identity. Perturbation of TET activity compromises embryo survival through dormancy; whereas its enhancement improves survival rates. Our results reveal the first essential chromatin regulator in establishing mammalian embryonic dormancy and pave the way to building its temporal regulatory code in embryonic and adult tissues.
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