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

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

PROVIDER: PRJNA813848 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18270958_1.fastq.gz	Fastqsanger.gz
	SRR18270958_2.fastq.gz	Fastqsanger.gz
	SRR18270959_1.fastq.gz	Fastqsanger.gz
	SRR18270959_2.fastq.gz	Fastqsanger.gz
	SRR18270960_1.fastq.gz	Fastqsanger.gz

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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

<i>Myh9</i> Plays an Essential Role in the Survival and Maintenance of Hematopoietic Stem/Progenitor Cells.

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. Our present study suggests an essential role for Myh9 in the survival and maintenance of HSPC in normal hematopoiesis.

| S-EPMC9221478 | biostudies-literature

Trappc1 is essential for naive T cell survival

Project description:Trappc1 is essential for naive T cell survival

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Non-muscle myosin heavy chain 9 maintains intestinal homeostasis by preventing epithelium necroptosis and colitis adenoma formation

Project description:Non-muscle myosin IIA plays an important role in cell adhesion, cell migration and tissue architecture. We previously showed that low activity of the heavy chain of non-muscle myosin II Myh9 is beneficial to Lgr5+ intestinal stem cell maintenance. However, the function of Myh9 in adult mouse intestinal epithelium is largely unclear. In this study, we used the inducible Villin-creERT2 knockout approach to delete Myh9 in adult mouse intestinal epithelium and observed that homozygous deletion of Myh9 causes colitis-like morphologic changes in intestine, leads to a high sensitivity to dextran sulfate sodium and promotes the colitis related adenomas formation in colon. Myh9 deletion disturbs cell junctions and impairs intestinal lumen barrier integrity, promoting the necroptosis of epithelial cells. Consistently, these changes can be partially rescued by Ripk3 knockout. Our results indicate that Myh9 is required for the maintenance of intestinal epithelium integrity and the prevention of cell necroptosis.

2021-03-20 | GSE169225 | GEO

Fibroblast-derived CSF1 is essential for intestinal macrophage maintenance

Project description:Fibroblast-derived CSF1 is essential for intestinal macrophage maintenance

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Epithelial EP4 plays an essential role in maintaining homeostasis in colon

Project description:Epithelial EP4 plays an essential role in maintaining homeostasis in colon

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MLL2, but not MLL1, plays a major role to sustain leukemia survival

Project description:MLL2, but not MLL1, plays a major role to sustain leukemia survival

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Bcl11a is essential for B-1a cell maintenance during aging

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MEAF6 is essential for proliferation and plays a role in the assembly of KAT7 complexes

Project description:MEAF6 is essential for proliferation and plays a role in the assembly of KAT7 complexes.

2020-09-23 | PXD020422 | JPOST Repository

Symmetric DNA Adenine Methylation Plays an Essential Role in Early-Diverging Fungi

Project description:Symmetric DNA Adenine Methylation Plays an Essential Role in Early-Diverging Fungi

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