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GFI1 maintains a chromatin state that is essential in human endothelial-to-hematopoietic transition

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE189802 | GEO | 2021/12/01

REPOSITORIES: GEO

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GFI1 regulates chromatin state essential in human endothelial-to-haematopoietic transition.

Project description:ObjectivesDuring embryonic haematopoiesis, haematopoietic stem/progenitor cells (HSPCs) develop from hemogenic endothelial cells (HECs) though endothelial to haematopoietic transition (EHT). However, little is known about how EHT is regulated in human. Here, we report that GFI1 plays an essential role in enabling normal EHT during haematopoietic differentiation of human embryonic stem cells (hESCs).ResultsGFI1 deletion in hESCs leads to a complete EHT defect due to a closed chromatin state of hematopoietic genes in HECs. Mechanically, directly regulates important signaling pathways essential for the EHT such as PI3K signaling.etc.ConclutionsTogether, our findings reveal an essential role of GFI1 mediated epigenetic mechanism underlying human EHT during hematopoiesis.

| S-EPMC9136496 | biostudies-literature

GFI1 maintains a chromatin state that is essential in human endothelial-to-hematopoietic transition [ATAC-seq]

Project description:During early embryonic hematopoiesis, hematopoietic stem/progenitor cells (HSPCs) are considered to develop from hemogenic endothelial cells (HECs) though endothelial to hematopoietic transition (EHT). However, little is known about how EHT is regulated in human. Here, we report that GFI1 plays an essential role in ensuring EHT during hematopoietic differentiation of human embryonic stem cells (hESCs). GFI1 deletion in hESCs showed a complete EHT defect due to a closed chromatin state of hematopoietic genes in HECs. Further analysis revealed that GFI1 directly binds and maintains the open chromatin state of genes important for EHT, such as PI3K signaling. Together, our findings reveal an essential role of GFI1 mediated epigenetic mechanism underlying human EHT during hematopoiesis.

2021-12-01 | GSE189799 | GEO

GFI1 maintains a chromatin state that is essential in human endothelial-to-hematopoietic transition [RNA-seq]

2021-12-01 | GSE189801 | GEO

GFI1 maintains a chromatin state that is essential in human endothelial-to-hematopoietic transition [CUT&TAG]

2021-12-01 | GSE189800 | GEO

GFI1 maintains a chromatin state that is essential in human endothelial-to-hematopoietic transition

Project description:GFI1 maintains a chromatin state that is essential in human endothelial-to-hematopoietic transition

| PRJNA784563 | ENA

GFI1 maintains a chromatin state that is essential in human endothelial-to-hematopoietic transition [CUT&TAG]

Project description:GFI1 maintains a chromatin state that is essential in human endothelial-to-hematopoietic transition [CUT&TAG]

| PRJNA784570 | ENA

GFI1 maintains a chromatin state that is essential in human endothelial-to-hematopoietic transition [RNA-seq]

Project description:GFI1 maintains a chromatin state that is essential in human endothelial-to-hematopoietic transition [RNA-seq]

| PRJNA784569 | ENA

GFI1 maintains a chromatin state that is essential in human endothelial-to-hematopoietic transition [ATAC-seq]

Project description:GFI1 maintains a chromatin state that is essential in human endothelial-to-hematopoietic transition [ATAC-seq]

| PRJNA784571 | ENA

Vitamin C–dependent lysine demethylase 6 (KDM6)-mediated demethylation promotes a chromatin state that supports the endothelial-to-hematopoietic transition

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

2019-07-22 | GSE132970 | GEO

Histone variant H3.3 maintains a decondensed chromatin state essential for mouse preimplantation development.

Project description:Histone variants can replace canonical histones in the nucleosome and modify chromatin structure and gene expression. The histone variant H3.3 preferentially associates with active chromatin and has been implicated in the regulation of a diverse range of developmental processes. However, the mechanisms by which H3.3 may regulate gene activity are unclear and gene duplication has hampered an analysis of H3.3 function in mouse. Here, we report that the specific knockdown of H3.3 in fertilized mouse zygotes leads to developmental arrest at the morula stage. This phenotype can be rescued by exogenous H3.3 but not by canonical H3.1 mRNA. Loss of H3.3 leads to over-condensation and mis-segregation of chromosomes as early as the two-cell stage, with corresponding high levels of aneuploidy, but does not appear to affect zygotic gene activation at the two-cell stage or lineage gene transcription at the morula stage. H3.3-deficient embryos have significantly reduced levels of markers of open chromatin, such as H3K36me2 and H4K16Ac. Importantly, a mutation in H3.3K36 that disrupts H3K36 methylation (H3.3K36R) does not rescue the H3.3 knockdown (KD) phenotype. In addition, H3.3 KD embryos have increased incorporation of linker H1. Knockdown of Mof (Kat8), an acetyltransferase specific for H4K16, similarly leads to excessive H1 incorporation. Remarkably, pan-H1 RNA interference (RNAi) partially rescues the chromosome condensation of H3.3 KD embryos and allows development to the blastocyst stage. These results reveal that H3.3 mediates a balance between open and condensed chromatin that is crucial for the fidelity of chromosome segregation during early mouse development.

| S-EPMC3742145 | biostudies-literature

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