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The histone acetyltransferase KAT6B is required for haematopoietic stem cell development and function

ABSTRACT: The histone acetyltransferase KAT6B is required for haematopoietic stem cell development and function

PROVIDER: PRJNA1077939 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28006100_1.fastq.gz	Fastqsanger.gz
	SRR28006100_2.fastq.gz	Fastqsanger.gz
	SRR28006077_1.fastq.gz	Fastqsanger.gz
	SRR28006077_2.fastq.gz	Fastqsanger.gz
	SRR28006078_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

The histone acetyltransferase KAT6B is required for haematopoietic stem cell development and function

Project description:The histone lysine acetyltransferase KAT6B (MYST4, MORF, QKF) is the target of recurrent chromosomal translocations causing haematological malignancies with poor prognosis. Using Kat6b germline deletion and overexpression in mice, we determined the role of KAT6B in the haematopoietic system. We found that KAT6B sustained the fetal haematopoietic stem cell pool but did not affect viability or differentiation. KAT6B was essential for normal levels of histone H3 lysine 9 (H3K9) acetylation but not for a previously proposed target, H3K23. Compound heterozygosity of Kat6b and the closely related gene, Kat6a, abolished haematopoietic reconstitution after transplantation. KAT6B and KAT6A cooperatively promoted transcription of genes regulating haematopoiesis, including the Hoxa cluster, Pbx1, Meis1, Gata family, Erg and Flt3. In conclusion, we identified the haematopoietic processes requiring Kat6b and showed that KAT6B and KAT6A synergistically promoted HSC development, function and transcription. Our findings are pertinent to current clinical trials testing KAT6A/B inhibitors as cancer therapeutics.

2024-02-25 | GSE256039 | GEO

Effects of loss and gain of the histone acetyltransferase KAT6B on DNA accessibility (ATAC-seq)

Project description:Heterozygous mutations in the histone acetyltransferase gene KAT6B (MYST4/MORF/QKF) cause cognitive disorders. Congruently, KAT6B is required for brain development, neural stem cell self-renewal and neuronal differentiation in mice. Despite the clear requirement for KAT6B in brain development, its molecular roles remain unexplored. Here we use ATAC sequencing to determine the effects of loss or gain of KAT6B on DNA accessiblity.

2024-11-06 | GSE267675 | GEO

Effects of loss and gain of KAT6B on gene expression in the developing cerebral cortex [Myst4_RNAseq]

Project description:High histone acetylation is associated with high transcriptional activity. The lysine acetyltransferase KAT6B is known to be required for histone acetylation and KAT6B is essential for normal brain development. In this study we examined the effects of loss and gain of KAT6B on gene expression in the developing cerebral cortex. We isolated RNA from the dorsal telencephalon of embryonic day 12.5 embryos, which is the primordium of the cerebral cortex, and from the E15.5 foetal cortex of mouse embryos and foetuses that lacked KAT6B or overexpressed KAT6B. Genes required for brain development and neuronal differentiation were downregulated in Kat6b null tissues and upregulated in Kat6b transgenic overexpressing tissue.

2024-11-06 | GSE280784 | GEO

Effects of loss and gain of KAT6B on gene expression in neural stem and progenitor cells [NSC_Kat6b_RNAseq]

Project description:High histone acetylation is associated with high transcriptional activity. The lysine acetyltransferase KAT6B is known to be required for histone acetylation and KAT6B is essential for normal brain development. In this study we examined the effects of loss and gain of KAT6B on gene expression in forebrain neural stem and progenitor cells (NSPCs). We isolated NSPCs from the dorsal telencephalon of embryonic day 12.5 embryos, which is the primordium of the cerebral cortex, from mouse embryos that lacked KAT6B or overexpressed KAT6B. We cultured the cells in vitro for 3 to 5 passages before isolating RNA for library production and RNA-sequencing. We found that genes required for neuronal differentiation and brain development were downregulated in Kat6b null cells and upregulated in Kat6b transgenic overexpressing cells.

2024-11-06 | GSE280783 | GEO

Epigenetic effects (H3K9ac, H3K14ac, H3K23ac and Pol II) of Kat6b loss in mouse neural stem cells (CUT&Tag)

Project description:Heterozygous mutations in the histone acetyltransferase gene KAT6B (MYST4/MORF/QKF) cause cognitive disorders. Congruently, KAT6B is required for brain development, neural stem cell self-renewal and neuronal differentiation in mice. Despite the clear requirement for KAT6B in brain development, its molecular roles remain unexplored. Here we use CUT&Tag sequencing to determine the effects of loss or gain of KAT6B on H3K9ac and H3K23ac histone marks and on RNA Pol II.

2024-11-06 | GSE267672 | GEO

Aging-Associated Decrease in the Histone Acetyltransferase KAT6B Causes Myeloid-Biased Hematopoietic Stem Cell Differentiation

Project description:Purpose: Gene expression profiling of long term hematopoietic stem cells (LT-HSCs) transduced with Kat6b shRNA and Non-Targeting Control (NTC)

2019-06-26 | GSE133304 | GEO

RNA sequencing of cortical neurons from Kat6b deficient mouse foetuses

Project description:The RNA sequencing data are part of a study reporting and investigating a mouse model of the Say-Barber-Biesecker-Young-Simpson (SBBYS) syndrome (OMIM:603736) and demonstrating proof-of-principle efficacy of postnatal treatment with sodium valproate (VPA) or acetyl-carnitine (ALCAR). The KAT6B gene encodes a histone lysine acetyltransferase. The RNA sequencing experiments identified genes that are differentially expressed between Vehicle treated Kat6b+/– and Kat6b+/+ cortical neurons and the subset genes that are restored to normal expression after treatment with ALCAR or VPA. Cortical neurons were isolated from four Kat6b+/– and four Kat6b+/+ E16.5 mouse cerebral cortex. Cells from each cortical neuron isolate were cultured with 1 mM ALCAR, 1 mM VPA or untreated medium (Vehicle) for 4 days.

2024-01-28 | GSE249964 | GEO

Aging-Associated Decrease in the Histone Acetyltransferase KAT6B Causes Myeloid-Biased Hematopoietic Stem Cell Differentiation

Project description:Aging-Associated Decrease in the Histone Acetyltransferase KAT6B Causes Myeloid-Biased Hematopoietic Stem Cell Differentiation

| PRJNA551021 | ENA

Effects of loss and gain of the histone acetyltransferase KAT6B on DNA accessibility (ATAC-seq)

Project description:Effects of loss and gain of the histone acetyltransferase KAT6B on DNA accessibility (ATAC-seq)

| PRJNA1112383 | ENA

Mutations in KAT6B, encoding a histone acetyltransferase, cause Genitopatellar syndrome.

Project description:Genitopatellar syndrome (GPS) is a skeletal dysplasia with cerebral and genital anomalies for which the molecular basis has not yet been determined. By exome sequencing, we found de novo heterozygous truncating mutations in KAT6B (lysine acetyltransferase 6B, formerly known as MYST4 and MORF) in three subjects; then by Sanger sequencing of KAT6B, we found similar mutations in three additional subjects. The mutant transcripts do not undergo nonsense-mediated decay in cells from subjects with GPS. In addition, human pathological analyses and mouse expression studies point to systemic roles of KAT6B in controlling organismal growth and development. Myst4 (the mouse orthologous gene) is expressed in mouse tissues corresponding to those affected by GPS. Phenotypic differences and similarities between GPS, the Say-Barber-Biesecker variant of Ohdo syndrome (caused by different mutations of KAT6B), and Rubinstein-Taybi syndrome (caused by mutations in other histone acetyltransferases) are discussed. Together, the data support an epigenetic dysregulation of the limb, brain, and genital developmental programs.

| S-EPMC3276659 | biostudies-literature

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