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ChIP-seq of ZMYM2-null and WT human ESCs

ABSTRACT: ChIP-seq of ZMYM2-null and WT human ESCs

PROVIDER: PRJEB33646 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR3449890.fastq.gz	Fastqsanger.gz
	ERR3449891.fastq.gz	Fastqsanger.gz
	ERR3449892.fastq.gz	Fastqsanger.gz
	ERR3449893.fastq.gz	Fastqsanger.gz
	ERR3449888.fastq.gz	Fastqsanger.gz

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ChIP-seq of ZMYM2-null and WT human ESCs

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DUX-miR-344-ZMYM2-mediated activation of MERVL LTRs induces a totipotent 2C-like state [ZMYM2 ChIP-seq]

Project description:Mouse embryonic stem cells (ESCs) sporadically express preimplantation two-cell-stage (2C) transcripts, including MERVL endogenous retrovirus and Zscan4 cluster genes. Such 2C-like cells (2CLCs) can contribute to both embryonic and extraembryonic tissues when reintroduced into early embryos. We examined global nucleosome occupancy and gene expression in 2CLCs and identified miR-344 as the noncoding molecule that positively controls 2CLC potency. We found that activation of endogenous MERVL or miR-344-2 alone is sufficient to induce 2CLCs with induction of 2C genes and an expanded potency. Mechanistically, miR-344 is activated by the 2C-state driver DUX and post-transcriptionally represses ZMYM2 and LSD1, which recruit the HDAC corepressor to MERVL LTR for transcriptional repression. Consistently, zygotic depletion of Zmym2 compromises the totipotency-to-pluripotency transition during early development. Our studies establish the novel DUX->miR-344--|Zmym2/Lsd1 axis that controls MERVL for expanded stem cell potency.

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ZMYM2-WT, ZMYM2-SIM2mut, and FOXO3 ChIP-seq in a U2OS stable cell line

Project description:Chromatin immuno-precipitation using anti-Flag (Sigma) or control IgG (Millipore) antibodies in a U2OS stable cell line. ZMYM2 has the synonym ZNF198. Note: paired-end sequencing libraires were created in this experiment but only the forward (R1) reads are available in this submission. The 'LIBRARY_LAYOUT' attribute is therefore set to be 'SINGLE' ather than 'PAIRED'.

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Mutation of ZMYM2 SIMs

Project description:The interaction between SUMO and ZMYM2 is mediated through specific motifs found in ZMYM2 that are called SIMs (SUMO interacting motifs). We found/characterised three SIMs in ZMYM2 and in vitro experiments showed that mutation in these residues prevent the interaction with SUMO. Microarray transcription profiling was done to study the effects of disrupting the multiSUMO binding activity of ZMYM2, assessing the differences in gene expression in cells expressing wild-type or SIM2 mutant version of ZMYM2.

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Project description:Mouse embryonic stem cells (ESCs) sporadically express preimplantation two-cell-stage (2C) transcripts, including MERVL endogenous retrovirus and Zscan4 cluster genes. Such 2C-like cells (2CLCs) can contribute to both embryonic and extraembryonic tissues when reintroduced into early embryos. We examined global nucleosome occupancy and gene expression in 2CLCs and identified miR-344 as the noncoding molecule that positively controls 2CLC potency. We found that activation of endogenous MERVL or miR-344-2 alone is sufficient to induce 2CLCs with induction of 2C genes and an expanded potency. Mechanistically, miR-344 is activated by the 2C-state driver DUX and post-transcriptionally represses ZMYM2 and LSD1, which recruit the HDAC corepressor to MERVL LTR for transcriptional repression. Consistently, zygotic depletion of Zmym2 compromises the totipotency-to-pluripotency transition during early development. Our studies establish the novel DUXmiR-344--|Zmym2/LsdSD1 axis that controls MERVL for expanded stem cell potency.

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