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RNA Sequencing Analysis of JFK-overexpressing and ING5-depleted HepG2 cells

ABSTRACT: RNA Sequencing Analysis of JFK-overexpressing and ING5-depleted HepG2 cells

PROVIDER: PRJNA699452 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13627909.fastq.gz	Fastqsanger.gz
	SRR13627910.fastq.gz	Fastqsanger.gz
	SRR13627911.fastq.gz	Fastqsanger.gz
	SRR13627912.fastq.gz	Fastqsanger.gz

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RNA Sequencing Analysis of JFK-overexpressing and ING5-depleted HepG2 cells

Project description:To explore the functional significance of JFK-mediated ING5 degradation, we performed genome-wide analysis of the transcriptome in hepatocytes that is regulated by the JFK-ING5 axis using RNA-based deep sequencing (RNA-seq). The data obtained from RNA-seq experiments were cross-analyzed with ChIP-seq data of ING5 from HepG2 cells.

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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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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.

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