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Genome-wide distribution of histone modification enzymes (KDM7A and UTX), histone modification (H3K9me2, H3K27me3, H3K4me3, H3K27ac), and transcription factor (p65) in TNF-alpha-stimulated human umbilical vein endothelial cell (HUVECs)

ABSTRACT: Genome-wide distribution of histone modification enzymes (KDM7A and UTX), histone modification (H3K9me2, H3K27me3, H3K4me3, H3K27ac), and transcription factor (p65) in TNF-alpha-stimulated human umbilical vein endothelial cell (HUVECs)

PROVIDER: PRJNA498996 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10875512.fastq.gz	Fastqsanger.gz
	SRR10875513.fastq.gz	Fastqsanger.gz
	SRR10875514.fastq.gz	Fastqsanger.gz
	SRR10875515.fastq.gz	Fastqsanger.gz
	SRR10875516.fastq.gz	Fastqsanger.gz

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Genome-wide distribution of histone modification enzymes (KDM7A and UTX), histone modification (H3K9me2, H3K27me3, H3K4me3, H3K27ac), and transcription factor (p65) in TNF-alpha-stimulated human umbilical vein endothelial cell (HUVECs)

Project description:Lysine 9 di-methylation and lysine 27 tri-methylation of histone H3 (H3K9me2 and H3K27me3) are mostly linked to gene repression. However, functions of repressive histone methylation dynamics during inflammatory responses remain poorly understood. Here, we show that lysine demethylase 7A (KDM7A) and 6A (UTX) are rapidly transported to nuclear factor kappa-B (NF-κB) related elements in human endothelial cells in response to tumor necrosis factor (TNF)-α. KDM7A and UTX demethylate H3K9me2 and H3K27me3, respectively, and cooperatively activate NF-κB dependent inflammatory genes. Furthermore, using both in situ Hi-C and other 3C based technology, loops between super enhancers (SEs) are newly formed following TNF-α-stimuli at NF-κB-dependent inflammatory loci where KDM7A- and UTX-recruitment coincide. Collectively, these findings suggest that erasing of repressive histone marks by KDM7A and UTX within NF-κB-related elements might functionally associate with formation of SE-SE three-dimensional interactions and could be a cue signal during inflammatory responses in human endothelial cells.

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Comparison of genome-wide distribution of histone modifications (H3K4me3, H3K9me2, H3K27me2, and H3K27me3) between wild-type and Kdm7a mutant embryos

Project description:Temporal and spatial colinear expression of Hox genes determines the specification of positional identities of the embryo. Post-translational modifications of histones contribute to transcriptional regulation, and are required for proper control of biological processes, including differentiation and development. Lysine demethylase 7A (Kdm7a) demethylates lysine 9 di-methylation of histone H3 (H3K9me2) and participates in transcriptional activation of developmental genes. However, the role of Kdm7a during mouse embryonic development remains to be elucidated. Here, we show that Kdm7a-/- mice exhibit anterior homeotic transformation of the axial skeleton (i.e. an increase in the number of presacral elements). Importantly, posterior Hox genes (caudally from Hox9) are specifically down-regulated in Kdm7a-/- embryos, which correlate with increased levels of H3K9me2. Taken together, these data suggest that Kdm7a is able to control transcription of posterior Hox genes, likely through its demethylating activity, and thereby regulating anterior-posterior development in mice.

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The Lysine Demethylase KDM7A Regulates Immediate Early Genes in Neurons.

Project description:Lysine demethylase KDM7A removes histone modifications H3K9me1/2 and H3K27me1/2. KDM7A plays critical roles in gene expression and contribute to biological processes including tumorigenesis, metabolism, and embryonic development. However, the functions of KDM7A in mammalian nervous system are still poorly explored. In this study, functional roles of KDM7A are comprehensively investigated in neuronal cells by applying CUT&Tag-seq, RNA-seq and mice models. Knockdown of Kdm7a in N2A cells result in the alteration of histone modifications near transcription start sites (TSSs) and the expression changes of a large number of genes. In particular, the expression of immediate early genes (IEGs), a series of genes maintaining the function of the nervous system and associating with neurological disorders, are significantly decreased upon Kdm7a knockdown. Furthermore, in vivo knockdown of Kdm7a in dentate gyrus (DG) neuron of mice hippocampus, via Adeno-associated virus (AAV)-based stereotaxic microinjection, led to a significant decrease of the expression of c-Fos, a marker of neuron activity. Behavior assays in mice further revealed that Kdm7a knockdown in hippocampus repress neuron activity, which leading to impairment of emotion and memory. Collectively, the study reveals that KDM7A affects neuron functions by regulating IEGs, which may provide new clues for understanding epigenetic mechanisms in neurological disorders.

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Project description:KDM7A Divergent Transcript (KDM7A-DT) is a stress-induced lncRNAs. In our previous studies, KDM7A-DT showed the most robust cellular phenotype alteration and a significant TP53-dependency upon oxidative and oncogenic stress induction. To investigate the functional roles of KDM7A-DT, we first performed overexpression experiments using fibroblasts. We found that MRC5 cells overexpressing KDM7A-DT escaped cell cycle proliferation and long-term survival ability and were associated with a distinct stress-related morphology (enlarged and flattened cells) compared to cells expressing just the vehicle control. To examine the effects of KDM7A-DT overexpression on the transcriptome, we performed a differential expression gene (DEG) analysis comparing a group of four independent biological replicates of MRC5 overexpressing KDM7A-DT to a group of samples from control cells.

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Project description:p65

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The lysine demethylase KDM7A regulates immediate early genes in neurons [CUT&Tag]

Project description:There are multiple post-translational modifications on amino acid residues at the N-terminus of histones that affect the structure of chromatin and alter the transcription of genes, thereby regulating a variety of biological processes. Lysine demethylase 7A (KDM7A) mainly removes histone modifications such as H3K9me1/2 and H3K27me1/2. Current research on KDM7A has focused on tumors, metabolism and development, while research on the function of the mammalian nervous system is still lacking. The functions and mechanisms of KDM7A in the regulation of neuronal cell differentiation and cell activity in the nervous system were investigated. Our study found that KDM7A regulates H3K9me2 and H3K27me2 but also affects other inhibitory or active histones, such as H3K9me3 and H3K27ac, thereby disturbing the transcription of some immediate early genes (IEGs) and consequently affecting the differentiation and activity of neuronal cells. IEGs are important for neuron cell proliferation, differentiation, formation of dendrites and neural circuit-related proteins, which are involved in maintaining the normal function of the nervous system. Imbalances in IEG expression have been found in some neurological disorders, such as depression and schizophrenia. Moreover, the changes in various histone modifications in neurodegenerative diseases and brain injury have recently received increasing attention. Therefore, our study provides a basis for revealing the epigenetic regulatory mechanisms of neurological disorders.

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