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Dynamic reorganization of nuclear architecture during human cardiogenesis

ABSTRACT: Dynamic reorganization of nuclear architecture during human cardiogenesis

PROVIDER: PRJNA417681 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6269200_1.fastq.gz	Fastqsanger.gz
	SRR6269200_2.fastq.gz	Fastqsanger.gz
	SRR6269250_1.fastq.gz	Fastqsanger.gz
	SRR6269250_2.fastq.gz	Fastqsanger.gz
	SRR6269201_1.fastq.gz	Fastqsanger.gz

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Dynamic reorganization of nuclear architecture during human cardiogenesis [RNA-seq]

Project description:Dynamic reorganization of nuclear architecture during human cardiogenesis [RNA-seq]

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Dynamic reorganization of nuclear architecture during human cardiogenesis [ATAC-seq]

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Dynamic reorganization of nuclear architecture during human cardiogenesis [HiC-seq]

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Dynamic reorganization of nuclear architecture during human cardiogenesis [ATAC-seq]

Project description:While chromosomal architecture varies among cell types, little is known about how this organization is established or its role in development. We integrated Hi-C, RNA-seq and ATAC-seq during cardiac differentiation from human pluripotent stem cells to generate a comprehensive profile of chromosomal architecture. We identified active and repressive domains that are dynamic during cardiogenesis and recapitulate in vivo cardiomyocytes. During differentiation, heterochromatic regions condense in cis. In contrast, many cardiac-specific genes, such as TTN (titin), transition to an active compartment coincident with upregulation. Moreover, we identify a network of genes, including TTN, that share the heart-specific splicing factor, RBM20, and become associated in trans during differentiation, suggesting the existence of a 3D nuclear splicing factory. Our results demonstrate both the dynamic nature in nuclear architecture and provide insights into how developmental genes are coordinately regulated.

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Dynamic reorganization of nuclear architecture during human cardiogenesis [RNA-seq]

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Chromatin architecture reorganization in somatic cell nuclear transfer embryos

Project description:Chromatin architecture reorganization in somatic cell nuclear transfer embryos

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Dynamic reorganization of nuclear architecture during human cardiogenesis

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-01-04 | GSE106690 | GEO

Chromatin architecture reorganization in somatic cell nuclear transfer embryos

Project description:The oocyte cytoplasm can reprogram somatic cell nucleus into a totipotent state but with low efficiency. The spatiotemporal chromatin organization of somatic cell nuclear transfer (SCNT) embryos remains elusive. Here, we examined higher-order chromatin structures of mouse SCNT embryos using an optimized low-input Hi-C approach. We found that the donor cell chromatin transformed to metaphase state rapidly after injection along with the dissolution of typical 3D chromatin structures. Intriguingly, the donor cell genome underwent a transition from mitotic metaphase-like state to meiosis metaphase II-like state within one hour after activation. Subsequently, weak chromatin compartments and topologically associating domains (TADs) emerged at 6 hours after activation. Then TADs were gradually removed until the 2-cell stage and then progressively reestablished. We found that relative few distal (> 2 Mb) interactions were present in 2-cell stage SCNT embryos. Also, obvious differences in compartment and TAD organization between fertilization-derived and SCNT embryos were observed in early stages (2-8 cell stages). Many interactions between super-enhancers and promoters were not successfully established in SCNT embryos, and these interactions were further shown important for zygotic genome activation (ZGA). Moreover, we demonstrate that the aberrant chromatin architecture reorganization in SCNT embryos may be due to the persistent H3K9me3 and can be partially rescued by the Kdm4d overexpression. This study therefore provides novel insight into chromatin architecture reorganization during SCNT embryo development.

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Lineage-specific reorganization of nuclear peripheral heterochromatin and H3K9me2 domains

Project description:Dynamic and regulated organization of chromatin within the 3-dimensional space of the nucleus has been postulated to contribute to gene accessibility, gene expression, and cell fate. Here we define the genome-wide lineage-specific reorganization of nuclear peripheral heterochromatin as a multipotent P19 embryocarcinoma cell adopts either a neural or a cardiac fate. We demonstrate that H3K9me2 marked nuclear peripheral heterochromatin undergoes lineage-specific local reorganization during cell fate determination. Lineage-specific loss of H3K9me2 is associated with spatial repositioning of genomic loci away from the nuclear periphery as shown by high-resolution 3D immuno-fluorescence in situ hybridization (3D immuno-FISH). The lineage-specific repositioning of loci away from the nuclear periphery is not always associated with activation of gene expression, but a subset of these genes is transcriptionally activated. Master regulator Mef2c is specifically repositioned from nuclear periphery during early neurogenic differentiation, but not early cardiogenic differentiation, with associated transcript upregulation. Master regulator Myocd is specifically repositioned during early cardiogenic differentiation, but not early neurogenic differentiation, and is transcriptionally upregulated at later stages of cardiac differentiation. These results provide experimental evidence for lineage-specific regulation of nuclear architecture when the same multipotent progenitor cell adopts distinct fates.

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