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

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

PROVIDER: PRJNA551021 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9601370.fastq.gz	Fastqsanger.gz
	SRR9601371.fastq.gz	Fastqsanger.gz
	SRR9601372.fastq.gz	Fastqsanger.gz
	SRR9601373.fastq.gz	Fastqsanger.gz
	SRR9601368.fastq.gz	Fastqsanger.gz

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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)

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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.

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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.

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Loss of KAT6B causes premature ossification and promotes osteoblast differentiation during development

Project description:The MYST family histone acetyltransferase gene, KAT6B (MYST4, MORF, QKF) is mutated in two distinct human congenital disorders characterised by intellectual disability, facial dysmorphogenesis and skeletal abnormalities, Say-Barber-Biesecker-Young-Simpson variant of Ohdo syndrome and Genitopatellar syndrome. Despite its requirement in normal skeletal development, the cellular and transcription effects of KAT6B in skeletogenesis have not been thoroughly studied. In this dataset, we examined the effects of loss of KAT6B on gene expression in proliferating primary mouse embryonic fibroblasts (MEFs) and MEFs induced to differentiated towards chondrocytes, osteoblasts and adipocytes. We show that loss of KAT6B in mesenchymal progenitor cells promotes transition towards an osteoblast-progenitor state with upregulation of gene targets of RUNX2, a master regulators of osteoblast development and concomitant downregulation of SOX9, a critical gene in chondrocyte development.

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RNA sequencing of cortical neurons from Kat6b deficient mouse foetuses

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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.

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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

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

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

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Loss of KAT6B causes premature ossification and promotes osteoblast differentiation during development

Project description:Loss of KAT6B causes premature ossification and promotes osteoblast differentiation during development

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