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RNA- and ATAC-seq data from hESCs differentiated with Wnt and Activin with or without CPI-203

ABSTRACT: RNA- and ATAC-seq data from hESCs differentiated with Wnt and Activin with or without CPI-203

PROVIDER: PRJNA735402 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14740635.fastq.gz	Fastqsanger.gz
	SRR14740636.fastq.gz	Fastqsanger.gz
	SRR14740637.fastq.gz	Fastqsanger.gz
	SRR14740638.fastq.gz	Fastqsanger.gz
	SRR14740639.fastq.gz	Fastqsanger.gz

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RNA- and ATAC-seq data from hESCs differentiated with Wnt and Activin with or without CPI-203

Project description:We report genome-wide changes in chromatin state and transcriptional output following Wnt-priming and subsequent Activin induced differentiation of human embryonic stem cell and the effects of BET bromodomain inhibition during Wnt-priming. The two signals, Wnt and Activin, although provided sequentially, result in stable mesendoderm differentiation (Yoney et al., 2018).

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Project description:Histones modulate gene expression by chromatin compaction, regulating numerous processes such as differentiation. However, the mechanisms underlying histone degradation remain elusive. When compared with their differentiated counterparts, immortal human embryonic stem cells (hESCs) have a unique chromatin architecture and low levels of trimethylated histone H3 at lysine 9 (H3K9me3), a heterochromatin-associated modification. Here we assess a link between the intrinsic epigenetic landscape and ubiquitin-proteasome system of hESCs. We find that hESCs exhibit high expression of UBE2K, a ubiquitin-conjugating enzyme. Loss of UBE2K increases the levels of H3K9 trimethyltransferase SETDB1, resulting in H3K9 trimethylation and repression of neurogenic genes during differentiation. Concomitantly, loss of UBE2K impairs the ability of hESCs to differentiate into neural progenitors with neurogenic properties. Besides H3K9 trimethylation, we find that UBE2K binds histone H3 to induce its polyubiquitination and degradation by the proteasome. Notably, ubc-20, the worm orthologue of UBE2K, also regulates both histone H3 levels and H3K9 trimethylation in C. elegans germline. Thus, our results indicate that UBE2K crosses evolutionary boundaries to promote histone H3 degradation and reduce H3K9me3 repressive marks in immortal cells.

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