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RNA sequencing data of Kat6a (Moz) mutant embryonic mouse hearts (ING4 and ING5 are essential for histone H3 lysine 14 acetylation and epicardial cell lineage development)

ABSTRACT: RNA sequencing data of Kat6a (Moz) mutant embryonic mouse hearts (ING4 and ING5 are essential for histone H3 lysine 14 acetylation and epicardial cell lineage development)

PROVIDER: PRJNA1032878 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26544480_1.fastq.gz	Fastqsanger.gz
	SRR26544480_2.fastq.gz	Fastqsanger.gz
	SRR26544481_1.fastq.gz	Fastqsanger.gz
	SRR26544481_2.fastq.gz	Fastqsanger.gz
	SRR26544482_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

RNA sequencing data of Kat6a (Moz) mutant embryonic mouse hearts (ING4 and ING5 are essential for histone H3 lysine 14 acetylation and epicardial cell lineage development)

Project description:Inhibitor of growth 4 and 5 (ING4 and ING5) are chromatin-binding proteins in the KAT6A, KAT6B and KAT7 histone acetyltransferase protein complexes. Heterozygous mutations in the KAT6A or KAT6B gene cause human disorders with cardiac defects, but the contribution of their chromatin adaptor proteins to development is unknown. We found that Ing5-/- mice had isolated cardiac ventricular septal defects. ING4 and ING5 are structurally similar proteins, suggesting a degree of redundancy. Combined loss of ING4 and ING5 caused developmental arrest at embryonic day E8.5, loss of histone H3 lysine 14 acetylation (H3K14ac) and a reduction in H3K23ac levels. Ing4+/-Ing5-/- hearts showed a paucity of epicardial cells and epicardium-derived cells, failure of myocardium compaction and coronary vasculature defects, accompanied by a reduction in the expression of epicardium genes. Our findings suggest that ING4 and ING5 are essential for heart development and promote epicardium and epicardium-derived cell fates and mutation of the human ING5 gene as a possible cause of isolated ventricular septal defects.

2024-02-01 | GSE246402 | GEO

RNA sequencing data of Ing4;Ing5 compound mutant embryonic mouse hearts (ING4 and ING5 are essential for histone H3 lysine 14 acetylation and epicardial cell lineage development)

2024-02-01 | GSE246403 | GEO

RNA sequencing data of Ing4;Ing5 double knock-out embryonic mouse hearts

Project description:Inhibitor of growth 4 and 5 (ING4 and ING5) are chromatin-binding proteins in the KAT6A, KAT6B and KAT7 histone acetyltransferase protein complexes. Heterozygous mutations in the KAT6A or KAT6B gene cause human disorders with cardiac defects, but the contribution of their chromatin adaptor proteins to development is unknown. We found that Ing5–/– mice had isolated cardiac ventricular septal defects. ING4 and ING5 are structurally similar proteins, suggesting a degree of redundancy. Combined loss of ING4 and ING5 caused developmental arrest at embryonic day E8.5, loss of histone H3 lysine 14 acetylation (H3K14ac), a reduction in H3K23ac levels and disruption of developmental gene expression in Ing4–/–Ing5–/– compared to control embryos. E12.5 Ing4+/–Ing5–/– hearts showed a paucity of epicardial cells and epicardium-derived cells, failure of myocardium compaction and coronary vasculature defects, accompanied by a reduction in the expression of epicardium genes compared to control hearts. In addition, a reduction in the expression of genes required for cell adhesion, both in whole E8.75 Ing4–/–Ing5–/– embryos and in E10.5 Ing4+/–Ing5–/– hearts compared to controls was observed. In vitro assessment of fibroblast and proepicardium explants revealed cell spreading and outgrowth defects. Our findings suggest that ING4 and ING5 are essential for heart development and promote epicardium and epicardium-derived cell fates and mutation of the human ING5 gene as a possible cause of isolated ventricular septal defects.

2024-02-01 | GSE252338 | GEO

RNA sequencing data of Ing4 Ing5 compound mutant embryonic mouse hearts (ING4 and ING5 are essential for histone H3 lysine 14 acetylation and epicardial cell lineage development)

Project description:RNA sequencing data of Ing4 Ing5 compound mutant embryonic mouse hearts (ING4 and ING5 are essential for histone H3 lysine 14 acetylation and epicardial cell lineage development)

| PRJNA1032879 | ENA

ING4 and ING5 are essential for histone H3 lysine 14 acetylation and epicardial cell lineage development

Project description:ING4 and ING5 are essential for histone H3 lysine 14 acetylation and epicardial cell lineage development

| PRJNA1032876 | ENA

The histone acetyltransferase KAT6A is recruited to unmethylated CpG islands via a DNA-binding winged helix domainThe histone acetyltransferase KAT6A is recruited to unmethylated CpG islands via a DNA-binding winged helix domain

Project description:The lysine acetyltransferase KAT6A (MOZ, MYST3) belongs to the MYST family of chromatin regulators, facilitating histone acetylation. Dysregulation of KAT6A has been implicated in developmental syndromes and the onset of acute myeloid leukemia (AML). Previous work suggests that KAT6A is recruited to its genomic targets by a combinatorial function of histone binding PHD fingers, transcription factors and chromatin binding interaction partners. Here, we demonstrated that a winged helix domain at the N-terminus of KAT6A specifically interacts with unmethylated CpG motifs. This DNA binding function leads to the association of KAT6A to unmethylated CpG islands (CGIs) genome wide. Mutation of the essential amino acids completely abrogates the enrichment of KAT6A at CGIs. Overexpression of a KAT6A WH1 mutant has a dominant negative effect on H3K9 histone acetylation, which is comparable to the effects upon overexpression of a KAT6A HAT domain mutant. Taken together, our work revealed a previously unrecognized chromatin recruitment mechanism of KAT6A, offering a new perspective on the role of KAT6A in gene regulation and human diseases

2023-01-14 | PXD034833 | Pride

A forward genetic screen for modifiers of transgene silencing in the mouse identifies Inhibitor of Growth Family Member 5 (Ing5)

Project description:Here we report the identification of a mutant allele of the Ing5 gene, also known as Inhibitor of Growth Family Member 5 and a member of the MOZ/MORF histone acetyltransferase complex. The mutation likely alters functionality of the Ing5 protein by inhibiting its ability to bind to its histone substrate, H3K4me3. We find that Ing5 acts as a suppressor of a multi-copy transgene reporter suggesting a complex role for Ing5 in regulating gene expression and show that Ing5 is required for normal embryonic development.

2019-01-14 | GSE76870 | GEO

RNA-seq profiling of mouse embryonic fibroblasts from Kat6a knockout and wildtype mice

Project description:Acetylation of histones by lysine acetyltransferases (KATs) is essential for transcriptional regulation of gene expression. The MYST family of KATs (KAT5-8) includes the oncogenes KAT6A (MOZ) and KAT6B (MORF/QKF). KAT6A has key roles in promoting cell proliferation through transcriptional activation of negative regulators of the Cdkn2a locus, which encode the tumor suppressors INK4A and ARF. To examine the loss of KAT6A function, mouse embryonic fibroblasts (MEFs) were isolated from E13.5 Kat6a+/+ and Kat6a–/– embryos and RNA-seq profiling was performed.

2018-08-03 | GSE108242 | GEO

RNA sequencing data of Ing4 Ing5 double knock-out embryonic mouse hearts

Project description:RNA sequencing data of Ing4 Ing5 double knock-out embryonic mouse hearts

| PRJNA1060248 | ENA

Gene Expression Profile of ING5-knockdown Brain Tumor Initiating Cell Lines

Project description:Transcriptome analysis on ING5-knockdown brain tumor stem cell lines Stem cell-like brain tumor initiating cells (BTICs) cause recurrence of glioblastomas, with BTIC "stemness" affected by epigenetic mechanisms. The ING family of epigenetic regulators (ING1-5) function by targeting histone acetyltransferase (HAT) or histone deacetylase (HDAC) complexes to the H3K4me3 mark to alter histone acetylation and subsequently, gene expression. Here we find that ectopic expression of ING5, the targeting subunit of HBO1, MOZ and MORF HAT complexes increases expression of the Oct4, Olig2 and Nestin stem cell markers, promotes self-renewal, prevents lineage differentiation and increases stem cell pools in BTIC populations. This activity requires the plant homeodomain region of ING5 that interacts specifically with the H3K4me3 mark. ING5 also enhances PI3K/AKT and MEK/ERK activity to sustain self-renewal of BTICs over serial passage of stem cell-like spheres. ING5 exerts these effects by activating transcription of calcium channel and follicle stimulating hormone (FSH) pathway genes. In silico analyses of The Cancer Genome Atlas (TCGA) data suggest that ING5 is a positive regulator of BTIC stemness, whose expression negatively correlates with patient prognosis, especially in the Proneural and Classical subtypes, and in tumors with low SOX2 expression. These data suggest that altering histone acetylation status and signaling pathways induced by ING5 may provide useful clinical strategies to target tumor resistance and recurrence in glioblastoma.

2017-06-24 | GSE100398 | GEO

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