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

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

PROVIDER: PRJNA549250 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9310282_1.fastq.gz	Fastqsanger.gz
	SRR9310282_2.fastq.gz	Fastqsanger.gz
	SRR9310283_1.fastq.gz	Fastqsanger.gz
	SRR9310283_2.fastq.gz	Fastqsanger.gz
	SRR9310284_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

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

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

| PRJNA549595 | ENA

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

Project description:Hematopoietic stem cells (HSCs)/progenitor cells (HPCs) are generated from hemogenic endothelial cells (HECs) during the endothelial-to-hematopoietic transition (EHT); however, the underlying mechanism remains poorly understood. Here, using an array of approaches, including CRSPR/Cas9 gene knockouts, RNA-Seq, ChIP-Seq, ATAC-Seq etc., we report that vitamin C (Vc) is essential in HPC generation during human pluripotent stem cell (hPSC) differentiation in defined culture conditions. Mechanistically, we found that the endothelial cells generated in the absence of Vc fail to undergo the EHT because of an apparent failure in opening up genomic loci essential for hematopoiesis. Under Vc deficiency, these loci exhibited abnormal accumulation of histone H3 trimethylation at Lys-27 (H3K27me3), a repressive histone modification that arose because of lower activities of demethylases that target H3K27me3. Consistently, deletion of the two H3K27me3 demethylases, Jumonji domain-containing 3 (JMJD3 or KDM6B) and histone demethylase UTX (UTX or KDM6A), impaired HPC generation even in the presence of Vc. Furthermore, we noted that Vc and jmjd3 are also important for HSC generation during zebrafish development. Together, our findings reveal an essential role for Vc in the EHT for hematopoiesis, and identify KDM6-mediated chromatin demethylation as an important regulatory mechanism in hematopoietic cell differentiation.

2019-07-22 | GSE132833 | GEO

KDM6 demethylase independent loss of histone H3 lysine 27 trimethylation during early embryonic development

Project description:H3K27me3 represses developmental genes at initial embryonic stages. The KDM6 family, comprised of UTX and JMJD3, are the only known proteins that demethylate H3K27me3 and they are hypothesized to catalyze the rapid removal of repressive chromatin in early mammalian development. However, we report that male embryos carrying mutations in both Utx and Jmjd3 survive to term and appear phenotypically normal at mid-gestation. We utilize several cell culture models to demonstrate that H3K27me3 is lost from repressed promoters in the absence of active KDM6 demethylation. Our data indicate that KDM6 H3K27me3 demethylation is not essential in the early embryo and that H3K27me3 loss from developmental genes occurs via novel mechanisms. Examination of 2 different histone modifications (H3K27me3 and H3K4me3) in 2 cell types (ES and retinoic acid treated ES cells) comparing WT to UTX and JMJD3 KOs. In ES cells, there are two WT replicates and two KO replicates, both measuring H3K27me3, and one replicate measuring input. In retinoic acid treatment, there are two replicates each for measuring H3K27me3 and H3K4me3 in WT and KO cell lines, and one replicate measuring input.

2014-06-12 | E-GEOD-58391 | biostudies-arrayexpress

KDM6 demethylase independent loss of histone H3 lysine 27 trimethylation during early embryonic development

2014-06-12 | GSE58391 | GEO

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

| S-EPMC6746450 | biostudies-literature

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

Depletion of demethylase KDM6 enhances early neuroectoderm commitment of human ESCs through inhibiting WNT activation

Project description:Epigenetic modifications play a crucial role in learning, memory and neurogenesis, but the study of its role in early neuroectoderm commitment from pluripotent inner cell mass is relatively lack. Here we utilized the system of directed neuroectoderm differentiation from human embryonic stem cells and identified KDM6B, an enzyme responsible to erase H3K27me3, was the most upregulated enzyme of histone methylation during neuroectoderm differentiation by transcriptome analysis. We then constructed KDM6B-null embryonic stem cells and found strikingly, the cells with KDM6B knockout exhibited much higher neuroectoderm induction efficiency. Furthermore, we constructed a serial of embryonic stem cell lines knocking out the other H3K27 demethylase KDM6A, and depleting both KDM6A and KDM6B, respectively. These cell lines together confirmed KDM6 impeded early neuroectoderm commitment. By RNA-seq, we found a panel of WNT activation genes significantly downregulated while WNT inhibiting genes significantly upregulated upon depletion of KDM6. Functional rescue assayed that WNT agonist could abolish the differential neuroectoderm induction due to manipulating KDM6 demonstrated WNT was the major downstream of KDM6 during early neural induction. Taken together, our findings illustrated the important role of histone methylation modifier KDM6A and KDM6B in neuroectoderm differentiation and provided additional insights into the precise epigenetic regulation in different stage of neurogenesis.

2021-09-29 | GSE172312 | GEO

Vitamin C dependent KDM6 demethylation specifies a functional chromatin state for endothelial-to-hematopoietic transition [ChIP-Seq]

Project description:Vitamin C dependent KDM6 demethylation specifies a functional chromatin state for endothelial-to-hematopoietic transition [ChIP-Seq]

| PRJNA549249 | ENA

Vitamin C dependent KDM6 demethylation specifies a functional chromatin state for endothelial-to-hematopoietic transition [RNA-Seq]

Project description:Vitamin C dependent KDM6 demethylation specifies a functional chromatin state for endothelial-to-hematopoietic transition [RNA-Seq]

| PRJNA549598 | ENA

KDM6 demethylase independent loss of histone H3 lysine 27 trimethylation during early embryonic development.

Project description:The early mammalian embryo utilizes histone H3 lysine 27 trimethylation (H3K27me3) to maintain essential developmental genes in a repressive chromatin state. As differentiation progresses, H3K27me3 is removed in a distinct fashion to activate lineage specific patterns of developmental gene expression. These rapid changes in early embryonic chromatin environment are thought to be dependent on H3K27 demethylases. We have taken a mouse genetics approach to remove activity of both H3K27 demethylases of the Kdm6 gene family, Utx (Kdm6a, X-linked gene) and Jmjd3 (Kdm6b, autosomal gene). Male embryos null for active H3K27 demethylation by the Kdm6 gene family survive to term. At mid-gestation, embryos demonstrate proper patterning and activation of Hox genes. These male embryos retain the Y-chromosome UTX homolog, UTY, which cannot demethylate H3K27me3 due to mutations in catalytic site of the Jumonji-C domain. Embryonic stem (ES) cells lacking all enzymatic KDM6 demethylation exhibit a typical decrease in global H3K27me3 levels with differentiation. Retinoic acid differentiations of these ES cells demonstrate loss of H3K27me3 and gain of H3K4me3 to Hox promoters and other transcription factors, and induce expression similar to control cells. A small subset of genes exhibit decreased expression associated with reduction of promoter H3K4me3 and some low-level accumulation of H3K27me3. Finally, Utx and Jmjd3 mutant mouse embryonic fibroblasts (MEFs) demonstrate dramatic loss of H3K27me3 from promoters of several Hox genes and transcription factors. Our results indicate that early embryonic H3K27me3 repression can be alleviated in the absence of active demethylation by the Kdm6 gene family.

| S-EPMC4125042 | biostudies-literature

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