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MYST4 (QKF/KAT6B/MORF) transcriptional targets in the adult dorsal cortex and E12.5 embryonic dorsal telencephalon

ABSTRACT: MYST4 (QKF/KAT6B/MORF) is an important regulator of brain development and function through its regulation of gene expression. Genetic targets of MYST4 are currently unknown. We have therefore carried out microarrays comparing gene expression in wild type and Qkf mouse tissues, namely the dorsal cortex and E12.5 dorsal telencephalon, to elucidate genetic targets of MYST4.

ORGANISM(S): Mus musculus

PROVIDER: GSE22969 | GEO | 2011/07/08

SECONDARY ACCESSION(S): PRJNA127743

REPOSITORIES: GEO

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MYST4 (QKF/KAT6B/MORF) transcriptional targets in the adult dorsal cortex and E12.5 embryonic dorsal telencephalon

Project description:MYST4 (QKF/KAT6B/MORF) is an important regulator of brain development and function through its regulation of gene expression. Genetic targets of MYST4 are currently unknown. We have therefore carried out microarrays comparing gene expression in wild type and Qkf mouse tissues, namely the dorsal cortex and E12.5 dorsal telencephalon, to elucidate genetic targets of MYST4. RNA was extracted for hybridization to arrays from 3 pairs of wild type and Qkf gt/gt mutant adult dorsal corticies and 3 pairs of wild type and Qkf gt/gt mutant E12.5 dorsal telencephalons

2011-07-08 | E-GEOD-22969 | biostudies-arrayexpress

Mus musculus

Project description:MYST4 (QKF/KAT6B/MORF) transcriptional targets in the adult dorsal cortex and E12.5 embryonic dorsal telencephalon

| PRJNA127743 | ENA

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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KAT6B overexpression rescues embryonic lethality in homozygous null KAT6A mice restoring vitality and normal lifespan [CUT&TAG]

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2025-02-24 | GSE287243 | GEO

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

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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.

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