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Genome-wide identification of transcriptional targets for ING5

ABSTRACT: Genome-wide identification of transcriptional targets for ING5

PROVIDER: PRJNA672296 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12905538_1.fastq.gz	Fastqsanger.gz
	SRR12905538_2.fastq.gz	Fastqsanger.gz
	SRR12905539_1.fastq.gz	Fastqsanger.gz
	SRR12905539_2.fastq.gz	Fastqsanger.gz

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Genome-wide identification of transcriptional targets for ING5

Project description:In this study, we performed chromatin immunoprecipitation-coupled massive parallel DNA sequencing (ChIP-seq) to analyze the genome-wide transcriptional profile of ING5 in hepatocytes. ChIP was performed first in HepG2 cells with antibodies against ING5. Following ChIP, ING5-associated DNAs were amplified using non-biased conditions, labeled, and sequenced with HiSeq 2500. The raw sequencing image data were examined by the Illumina analysis pipeline, aligned to the unmasked human reference genome (GRCh37, hg19) using Bowtie2, and further analyzed by MACS (Model-based Analysis for ChIP-Seq).

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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.

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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: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.

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