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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)

2019-06-26 | GSE133304 | 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

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

Aging-associated decrease in the histone acetyltransferase KAT6B is linked to altered hematopoietic stem cell differentiation.

Project description:Aged hematopoietic stem cells (HSCs) undergo biased lineage priming and differentiation toward production of myeloid cells. A comprehensive understanding of gene regulatory mechanisms causing HSC aging is needed to devise new strategies to sustainably improve immune function in aged individuals. Here, a focused short hairpin RNA screen of epigenetic factors reveals that the histone acetyltransferase Kat6b regulates myeloid cell production from hematopoietic progenitor cells. Within the stem and progenitor cell compartment, Kat6b is highly expressed in long-term (LT)-HSCs and is significantly decreased with aging at the transcript and protein levels. Knockdown of Kat6b in young LT-HSCs causes skewed production of myeloid cells at the expense of erythroid cells both in vitro and in vivo. Transcriptome analysis identifies enrichment of aging and macrophage-associated gene signatures alongside reduced expression of self-renewal and multilineage priming signatures. Together, our work identifies KAT6B as a novel epigenetic regulator of hematopoietic differentiation and a target to improve aged immune function.

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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

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

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

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

| PRJNA1077939 | ENA

Identification of KAT6B signature on KAT6B deficient SCLC cell Lines

Project description:To develop our gene expression experiment, we have employed whole genome microarray expression profiling as a discovery platform to identify genes potentially regulated by the transcriptional coactivator KAT6B. Expression of KAT6B gene was downregulated in two human SCLC cell lines using two different short hairpin RNAs. RNAs from these modified cell lines were hybridized in Agilent platform.

2015-10-07 | GSE59136 | GEO

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