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Mechanoresponsive genomic enhancers potentiate the cellular response to matrix stiffness [MYH9 facs}

ABSTRACT: Mechanoresponsive genomic enhancers potentiate the cellular response to matrix stiffness [MYH9 facs}

PROVIDER: PRJNA1019772 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26138849.fastq.gz	Fastqsanger.gz
	SRR26138850.fastq.gz	Fastqsanger.gz
	SRR26138851.fastq.gz	Fastqsanger.gz
	SRR26138852.fastq.gz	Fastqsanger.gz
	SRR26138853.fastq.gz	Fastqsanger.gz

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Mechanoresponsive genomic enhancers potentiate the cellular response to matrix stiffness

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Mechanoresponsive genomic enhancers potentiate the cellular response to matrix stiffness [migration]

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Mechanoresponsive genomic enhancers potentiate the cellular response to matrix stiffness [ATAC-seq]

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Mechanoresponsive genomic enhancers potentiate the cellular response to matrix stiffness [scRNA-seq]

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Mechanoresponsive genomic enhancers potentiate the cellular response to matrix stiffness [Bulk RNA-seq]

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Mechanoresponsive genomic enhancers potentiate the cellular response to matrix stiffness [MYH9 facs}

Project description:Epigenetic control of gene regulation and cell phenotype is influenced by changes in the mechanical microenvironment. Yet how mechanical forces precisely influence epigenetic state to regulate transcriptional responses remains largely unmapped. Here, we combine genome-wide epigenome profiling, epigenome editing, and phenotypic and single-cell RNA-seq screening to identify a sub-class of genomic enhancers that is responsive to the mechanical microenvironment. These enhancers regulate genes that act as key drivers for a variety of functional behaviors including apoptosis, mechanotransduction, proliferation, and migration. We find distinct patterns wherein subsets of mechano-enhancers can be preferentially active on either soft or stiff extracellular matrix (ECM) contexts. Epigenetic editing of these mechano-enhancers on rigid materials precisely tunes mechanically-induced gene expression to levels observed on softer materials, and broadly enables reprogramming of cellular response to the mechanical microenvironment. These mechanically-activated enhancers act as key signal transducers and may constitute a new class of targets that can be modulated to alter mechanically-driven disease states.

2024-01-31 | GSE243761 | GEO

Mechanoresponsive genomic enhancers potentiate the cellular response to matrix stiffness

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

2024-01-31 | GSE243765 | GEO

Myh9 plays essential role in hematopoietic stem/progenitor cells survival and maintenance

Project description:Myosin heavy chain 9 (MYH9) gene encodes a protein named non-muscle heavy chain IIA (NMHC IIA), interacting with actin and participating in various biological processes. Mutations in MYH9 cause an array of autosomal dominant disorders, known as MYH9-related diseases (MYH9-RD). However, the role of MYH9 in normal hematopoiesis remains largely unexplored. By using Mx1-cre Myh9 conditional knockout mice, we established an inducible system to precisely inactivate Myh9 function in hematopoietic cells in vivo. The results showed that deletion of Myh9 led to severe defects in hematopoiesis, characterized by pancytopenia, drastic decreases of hematopoietic stem/progenitor cells (HSPC), and bone marrow failure, causing early lethality in mice. The defect in hematopoiesis caused by Myh9 ablation is cell autonomous. In addition, Myh9 deletion impairs HSPC repopulation capacity and increases apoptosis. RNA sequencing results revealed significant alterations in the expression of genes related to HSC self-renewal and maintenance, while multiple signal pathways were also involved, including genes for HSC and myeloid cell development, intrinsic apoptosis, targets of mTOR signaling, and maturity of hematopoietic cells. Collectively, our findings suggest an essential role for Myh9 in the survival and maintenance of HSPC in normal hematopoiesis.

2022-06-01 | GSE198134 | GEO

Mechanoresponsive genomic enhancers potentiate the cellular response to matrix stiffness [migration]

2024-01-31 | GSE243760 | GEO