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TETs controls maintenance DNA methylation via the regulation of Dppa3

ABSTRACT: TETs controls maintenance DNA methylation via the regulation of Dppa3

PROVIDER: PRJEB35009 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR3607090.fastq.gz	Fastqsanger.gz
	ERR3607100.fastq.gz	Fastqsanger.gz
	ERR3607110.fastq.gz	Fastqsanger.gz
	ERR3607091.fastq.gz	Fastqsanger.gz
	ERR3607101.fastq.gz	Fastqsanger.gz

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Tet1 controls maintenance DNA methylation via the regulation of Dppa3

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DNA methylation profiling to investigate how Tet1 controls maintenance DNA methylation via the regulation of Dppa3 in ESCs

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LINE-1 DNA methylation levels in DPPA3 KO overexpressing DPPA3 mutants

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TETs controls maintenance DNA methylation via the regulation of Dppa3

Project description:Dissection of catalytic and non-catalytic functions of Tet1 and Tet2. Transcriptome profiling of wild type, Tet1 catalytic mutants, Tet2 and Tet1/2 catalytic mutant catalytic during EpiLC differentiation.

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ChIP-MS of DPPA3/STELLA in mouse embryonic stem cells

Project description:Genome-wide DNA demethylation is a unique feature of mammalian development and naïve pluripotent stem cells. So far, it was unclear how mammals specifically achieve global DNA hypomethylation, given the high conservation of the DNA (de-)methylation machinery among vertebrates. We found that DNA demethylation requires TET activity but mostly occurs at sites where TET proteins are not bound suggesting a rather indirect mechanism. Among the few specific genes bound and activated by TET proteins was the naïve pluripotency and germline marker Dppa3 (Pgc7, Stella), which undergoes TDG dependent demethylation. The requirement of TET proteins for genome-wide DNA demethylation could be bypassed by ectopic expression of Dppa3. We show that DPPA3 binds and displaces UHRF1 from chromatin and thereby prevents the recruitment and activation of the maintenance DNA methyltransferase DNMT1. We demonstrate that DPPA3 alone can drive global DNA demethylation when transferred to amphibians (Xenopus) and fish (medaka), both species that naturally do not have a Dppa3 gene and exhibit no post-fertilization DNA demethylation. Our results show that TET proteins are responsible for active and - indirectly also for - passive DNA demethylation; while TET proteins initiate local and gene-specific demethylation in vertebrates, the recent emergence of DPPA3 introduced a unique means of genome-wide passive demethylation in mammals and contributed to the evolution of epigenetic regulation during early mammalian development.

2020-10-12 | PXD019794 | Pride

DPPA3-HIF1a axis controls colorectal cancer chemoresistance by imposing a slow cell-cycle phenotype (DNA methylation arrays)

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Project description:Distinct cell types emerge from embryonic stem cells through a precise and coordinated execution of gene expression programs during lineage commitment. This is established by the action of lineage specific transcription factors along with chromatin complexes. Numerous studies focused on epigenetic factors that affect ESC self-renewal and pluripotency. Through our laboratory's previous studies on ESCs pluripotency, we found that Dppa3, as a Naive state marker gene, is of great significance to the transformation of mESCs pluripotency. However, the influence of overexpression of Dppa3 in ESCs on mESCs status has not been determined. Our results show that overexpression of Dppa3 induces global DNA demethylation, which is beneficial to the maintenance of pluripotency, but its differentiation ability is significantly impaired. In mESCs, Dppa3 regulates mESCs pluripotency by inhibiting de novo methylation pathway, maintaining methylation pathway, promoting demethylation pathway Tet2, up-regulating active histone modification and down-regulating heterogeneous histone modification. The 2C-like state of ESCs recapitulates key aspects of the two-cell stage mouse embryo both phenotypically and molecular, which providing a cellular model to investigate the progress of ZGA. Our results found Dppa3 promote facilitate 2C-state conversion.

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