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Relaxed 3D genome conformation facilitates the pluripotent to totipotent-like state transition in embryonic stem cells

ABSTRACT: Relaxed 3D genome conformation facilitates the pluripotent to totipotent-like state transition in embryonic stem cells

PROVIDER: PRJNA669845 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12842427_1.fastq.gz	Fastqsanger.gz
	SRR12842427_2.fastq.gz	Fastqsanger.gz
	SRR12842428_1.fastq.gz	Fastqsanger.gz
	SRR12842428_2.fastq.gz	Fastqsanger.gz
	SRR12842429_1.fastq.gz	Fastqsanger.gz

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Relaxed 3D genome conformation facilitates the pluripotent to totipotent-like state transition in embryonic stem cells

Project description:The 3D genome organization is crucial for gene regulation. Although recent studies have revealed a uniquely relaxed genome conformation in totipotent early blastomeres of both fertilized and cloned embryos, how weakened higher-order chromatin structure is functionally linked to totipotency acquisition remains elusive. Using low-input Hi-C, ATAC-seq, and ChIP-seq, we systematically examined the dynamics of 3D genome and epigenome during pluripotent to totipotent-like state transition in mouse embryonic stem cells (ESCs). The spontaneously converted 2-cell-embryo-like cells (2CLCs) exhibited more relaxed chromatin architecture compared to ESCs, including global weakening of both enhancer-promoter interactions and TAD insulation. While the former correlated with inactivation of ESC enhancers and down-regulation of pluripotent genes, the latter might facilitate contacts between the putative new enhancers arising in 2CLCs and neighboring 2C genes. Importantly, disruption of chromatin organization by depleting CTCF or the cohesin complex promoted the ESC to 2CLC transition. Our results thus establish a critical role of 3D genome organization in totipotency acquisition.

2021-10-20 | GSE159623 | GEO

Relaxed 3D genome conformation facilitates the pluripotent to totipotent-like state transition in embryonic stem cells [Hi-C]

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Relaxed 3D genome conformation facilitates the pluripotent to totipotent-like state transition in embryonic stem cells [ATAC-seq, ChIP-seq, RNA-seq, CUT&Tag]

2021-10-20 | GSE159621 | GEO

Relaxed 3D genome conformation facilitates the pluripotent to totipotent-like state transition in embryonic stem cells [Hi-C]

Project description:Relaxed 3D genome conformation facilitates the pluripotent to totipotent-like state transition in embryonic stem cells [Hi-C]

| PRJNA669874 | ENA

Relaxed 3D genome conformation facilitates the pluripotent to totipotent-like state transition in embryonic stem cells [ATAC-seq, ChIP-seq, RNA-seq, CUT&Tag]

Project description:Relaxed 3D genome conformation facilitates the pluripotent to totipotent-like state transition in embryonic stem cells [ATAC-seq, ChIP-seq, RNA-seq, CUT&Tag]

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Relaxed 3D genome conformation facilitates the pluripotent to totipotent-like state transition in embryonic stem cells.

Project description:The 3D genome organization is crucial for gene regulation. Although recent studies have revealed a uniquely relaxed genome conformation in totipotent early blastomeres of both fertilized and cloned embryos, how weakened higher-order chromatin structure is functionally linked to totipotency acquisition remains elusive. Using low-input Hi-C, ATAC-seq and ChIP-seq, we systematically examined the dynamics of 3D genome and epigenome during pluripotent to totipotent-like state transition in mouse embryonic stem cells (ESCs). The spontaneously converted 2-cell-embryo-like cells (2CLCs) exhibited more relaxed chromatin architecture compared to ESCs, including global weakening of both enhancer-promoter interactions and TAD insulation. While the former correlated with inactivation of ESC enhancers and down-regulation of pluripotent genes, the latter might facilitate contacts between the putative new enhancers arising in 2CLCs and neighboring 2C genes. Importantly, disruption of chromatin organization by depleting CTCF or the cohesin complex promoted the ESC to 2CLC transition. Our results thus establish a critical role of 3D genome organization in totipotency acquisition.

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NAT10-mediated β-hydroxybutyrylation Rewires Genomic 3D Conformation and Replication Timing

Project description:Spatiotemporal regulation of chromatin replication (replication timing, RT） in eukaryotes is critical to maintain the genomic integrity. Here we focused on epigenetic mechanisms in rewiring genomic 3D conformation and replication timing. The results show that the novel lysine β-hydroxybutyrylation (Kbhb) modifications accelerates chromatin replication without inducing replication defects. This effect was mediated by the NAT10, a novel b-hydroxybutyryl-transferase, through regulating the association of NAT10 and CTCF with chromatin. Depletion of NAT10 and NAT10-mediated Kbhb dramatically reduce chromatin-bound NAT10 and CTCF, resulting in reorganization of genomic 3D conformation with enhanced trans- and cis-interaction in Hi-C matrix, with elevated proportion of A compartments, and with reorganized TADs boundaries. Moreover, reorganization of genomic 3D conformation contributes to rewire replication timing. These results support models in which NAT10-mediated β-hydroxybutyrylation coordinates genomic 3D conformation reorganization with replication timing alteration, and emphatically address the concept that epigenetic mechanisms reconcile genomic 3D conformation with replication timing.

2021-09-08 | GSE175731 | GEO

NAT10-mediated β-hydroxybutyrylation Rewires Genomic 3D Conformation and Replication Timing [Replication-seq]

Project description:Spatiotemporal regulation of chromatin replication (replication timing, RT) in eukaryotes is critical to maintain the genomic integrity. Here we focused on epigenetic mechanisms in rewiring genomic 3D conformation and replication timing. The results show that the novel lysine β-hydroxybutyrylation (Kbhb) modifications accelerates chromatin replication without inducing replication defects. This effect was mediated by the NAT10, a novel b-hydroxybutyryl-transferase, through regulating the association of NAT10 and CTCF with chromatin. Depletion of NAT10 and NAT10-mediated Kbhb dramatically reduce chromatin-bound NAT10 and CTCF, resulting in reorganization of genomic 3D conformation with enhanced trans- and cis-interaction in Hi-C matrix, with elevated proportion of A compartments, and with reorganized TADs boundaries. Moreover, reorganization of genomic 3D conformation contributes to rewire replication timing. These results support models in which NAT10-mediated β-hydroxybutyrylation coordinates genomic 3D conformation reorganization with replication timing alteration, and emphatically address the concept that epigenetic mechanisms reconcile genomic 3D conformation with replication timing.

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NAT10-mediated β-hydroxybutyrylation Rewires Genomic 3D Conformation and Replication Timing [Hi-C]

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Myc and Dnmt1 impede the pluripotent to totipotent state transition in embryonic stem cell [RRBS]

Project description:Totipotency is defined as the ability of a cell to generate all the cell types of an organism, including those of the extraembryonic tissues. Unlike pluripotency, the molecular features and the establishment of totipotency are poorly understood. In mouse embryonic stem cell (ESC) culture, a small percentage of cells transits into a totipotent state by expressing a group of genes that are only expressed in 2-cell-stage embryos. To understand how this transition takes place, we performed single cell RNA-seq analysis which revealed a two-step transcriptional reprogramming process characterized by downregulation of pluripotent genes in the first step and upregulation of the 2-cell embryo-specific genes in the second step. To identify factors controlling the transition process, we performed a CRISPR/Cas9-mediated genetic screen which revealed Myc and Dnmt1 as two factors preventing the transition. Mechanistic studies demonstrate that Myc prevents down-regulation of the genes in the first step, while Dnmt1 impedes gene activation in the second step. Collectively, our study reveals insights into the mechanism underlying establishment and regulation of totipotent state in ESCs.

2019-04-12 | GSE121458 | GEO

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