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

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

PROVIDER: PRJNA549598 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9326240_1.fastq.gz	Fastqsanger.gz
	SRR9326240_2.fastq.gz	Fastqsanger.gz
	SRR9326231_1.fastq.gz	Fastqsanger.gz
	SRR9326231_2.fastq.gz	Fastqsanger.gz
	SRR9326241_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

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 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

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

Project description:Hematopoietic stem/progenitor cells (HSPCs) are generated from hemogenic endothelial cells (HECs) through endothelial-to-hematopoietic transition (EHT); however, the underlying mechanism remains poorly understood. Here, we report that HPC generation is significantly reduced in hPSC differentiatiation in a defined condition without vitamin C (Vc). Mechanistically, the endothelial cells generated in the absence of Vc fail to undergo EHT due to apparent failure in opening genomic loci essential for hematopoiesis. These loci exhibit abnormal accumulation of H3K27me3, a repressive histone modification due to lower activity of its demethylases. Consistently, deletion of H3K27me3 demethylases, JMJD3 and UTX, impaires HPC generation in the presence of Vc. Furthermore, Vc and jmjd3 are also important for HSC generation during zebrafish development. Together, we reveal an obligatory role of Vc underlying EHT process in hematopoisis and further support the important function of Vc during development.

2019-07-22 | GSE132969 | GEO

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

2019-07-22 | GSE132834 | GEO

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

| PRJNA549250 | ENA

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

| S-EPMC6746450 | biostudies-literature

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 Induces Specific Demethylation of H3K9me2 in Mouse Embryonic Stem Cells via Kdm3a/b

Project description:Histone methylation patterns regulate gene expression and are highly dynamic during development. The erasure of histone methylation is carried out by histone demethylase enzymes. We had previously shown that vitamin C enhances the activity of Tet enzymes in embryonic stem (ES) cells, leading to DNA demethylation and activation of germline genes. We report here that vitamin C induces a remarkably specific demethylation of histone H3 lysine 9 dimethylation (H3K9me2) in ES cells. Vitamin C treatment reduces global levels of H3K9me2, but not other histone methylation marks analyzed, as measured by Western blot, immunofluorescence and mass spectrometry. Vitamin C leads to widespread loss of H3K9me2 at large chromosomal domains as well as gene promoters and repeat elements. Vitamin C-induced loss of H3K9me2 occurs rapidly within 24 hours and is reversible. Importantly, we found that the histone demethylases Kdm3a and Kdm3b are required for vitamin C-induced demethylation of H3K9me2. Moreover, we show that vitamin C-induced Kdm3a/b-mediated H3K9me2 demethylation and Tet-mediated DNA demethylation are independent processes. Lastly, we document Kdm3a/b are partially required for the up-regulation of germline genes by vitamin C. These results reveal a specific role for vitamin C in histone demethylation in ES cells, and document that DNA methylation and H3K9me2 cooperate to silence germline genes in pluripotent cells.

2017-06-30 | GSE84009 | GEO

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