Parallel analysis of H3K9ac reveals Dux-dependent 2C activation deficiency in mouse SCNT embryos
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA600888 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10876841_1.fastq.gz | Fastqsanger.gz | |||
| SRR10876841_2.fastq.gz | Fastqsanger.gz | |||
| SRR10876842_1.fastq.gz | Fastqsanger.gz | |||
| SRR10876842_2.fastq.gz | Fastqsanger.gz | |||
| SRR10876843_1.fastq.gz | Fastqsanger.gz |
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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 DUX->miR-344--|Zmym2/Lsd1 axis that controls MERVL for expanded stem cell potency.
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