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Nuclear Deformation Guides Chromatin Reorganization in Cardiac Development and Disease

ABSTRACT: Nuclear Deformation Guides Chromatin Reorganization in Cardiac Development and Disease

PROVIDER: PRJNA739991 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14879946_1.fastq.gz	Fastqsanger.gz
	SRR14879946_2.fastq.gz	Fastqsanger.gz
	SRR14879947_1.fastq.gz	Fastqsanger.gz
	SRR14879947_2.fastq.gz	Fastqsanger.gz
	SRR14879948_1.fastq.gz	Fastqsanger.gz

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Nuclear Deformation Guides Chromatin Reorganization in Cardiac Development and Disease

Project description:The purpose of this study was to understand the how the supression of H3K9me3 impacts the phenotype of cardiac cells. Therefore, we compared the mRNA expression profiles of cardiac cells isolated from H3K9M (inducible histone H3.3 lysine-to-methionine mutant) and H3WT (inducibly expressed wild-type H3.3) cells.

2022-07-27 | GSE178674 | GEO

Nuclear deformation guides chromatin reorganization in cardiac development and disease.

Project description:In cardiovascular tissues, changes in the mechanical properties of the extracellular matrix are associated with cellular de-differentiation and with subsequent functional declines. However, the underlying mechanoreceptive mechanisms are largely unclear. Here, by generating high-resolution, full-field strain maps of cardiomyocyte nuclei during contraction in vitro, complemented with evidence from tissues from patients with cardiomyopathy and from mice with reduced cardiac performance, we show that cardiomyocytes establish a distinct nuclear organization during maturation, characterized by the reorganization of H3K9me3-marked chromatin towards the nuclear border. Specifically, we show that intranuclear tension is spatially correlated with H3K9me3-marked chromatin, that reductions in nuclear deformation (through environmental stiffening or through the disruption of complexes of the linker of nucleoskeleton and cytoskeleton) abrogate chromatin reorganization and lead to the dissociation of H3K9me3-marked chromatin from the nuclear periphery, and that the suppression of H3K9 methylation induces chromatin reorganization and reduces the expression of cardiac developmental genes. Overall, our findings indicate that, by integrating environmental mechanical cues, the nuclei of cardiomyocytes guide and stabilize the fate of cells through the reorganization of epigenetically marked chromatin.

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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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Dynamic reorganization of nuclear architecture during human cardiogenesis

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