Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ANP32E Restricts Widespread Chromatin Accessibility Through Regulation of H2A.Z

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE145705 | GEO | 2020/09/08

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

ANP32E Restricts Widespread Chromatin Accessibility Through Regulation of H2A.Z [RNA-seq]

Project description:Genome-wide chromatin state underlies gene expression potential and cellular function. Epigenetic features and nucleosome positioning are major factors in determining chromatin accessibility. Our study investigates how genomic localization of the histone variant H2A.Z regulates chromatin state in mouse fibroblasts. We define H2A.Z as a universal chromatin accessibility factor, and demonstrate that ANP32E antagonizes H2A.Z accumulation to restrict chromatin accessibility genome-wide. In the absence of ANP32E, H2A.Z accumulates in a hierarchical manner at promoters. H2A.Z initially localizes at the +1 nucleosome, and then if H2A.Z is already present at the +1 nucleosome position in WT, additional H2A.Z accumulates at the -1 nucleosome position. This hierarchical H2A.Z accumulation coincides with improved nucleosome positioning, heightened transcription factor footprint protection, and increased expression for neighboring genes. Thus, ANP32E dramatically influences genome-wide chromatin accessibility through refinement of H2A.Z patterns, providing a means to reprogram chromatin state and to hone gene expression levels.

2020-09-08 | GSE145704 | GEO

ANP32E Restricts Widespread Chromatin Accessibility Through Regulation of H2A.Z

Project description:ANP32E Restricts Widespread Chromatin Accessibility Through Regulation of H2A.Z

| PRJNA607979 | ENA

ANP32E Restricts Widespread Chromatin Accessibility Through Regulation of H2A.Z [RNA-seq]

Project description:ANP32E Restricts Widespread Chromatin Accessibility Through Regulation of H2A.Z [RNA-seq]

| PRJNA608061 | ENA

Genome-wide chromatin accessibility is restricted by ANP32E.

Project description:Genome-wide chromatin state underlies gene expression potential and cellular function. Epigenetic features and nucleosome positioning contribute to the accessibility of DNA, but widespread regulators of chromatin state are largely unknown. Our study investigates how coordination of ANP32E and H2A.Z contributes to genome-wide chromatin state in mouse fibroblasts. We define H2A.Z as a universal chromatin accessibility factor, and demonstrate that ANP32E antagonizes H2A.Z accumulation to restrict chromatin accessibility genome-wide. In the absence of ANP32E, H2A.Z accumulates at promoters in a hierarchical manner. H2A.Z initially localizes downstream of the transcription start site, and if H2A.Z is already present downstream, additional H2A.Z accumulates upstream. This hierarchical H2A.Z accumulation coincides with improved nucleosome positioning, heightened transcription factor binding, and increased expression of neighboring genes. Thus, ANP32E dramatically influences genome-wide chromatin accessibility through subtle refinement of H2A.Z patterns, providing a means to reprogram chromatin state and to hone gene expression levels.

| S-EPMC7546623 | biostudies-literature

Nfib promotes Metastasis through a Widespread Increase in Chromatin Accessibility

Project description:This SuperSeries is composed of the SubSeries listed below.

2016-05-10 | GSE81258 | GEO

UpSET Recruits HDAC Complexes and Restricts Chromatin Accessibility and Acetylation at Promoter Regions

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2012-12-07 | E-GEOD-34720 | biostudies-arrayexpress

Hypoxia-mediated regulation of DDX5 through decreased chromatin accessibility and post-translational targeting restricts R-loop accumulation.

Project description:Local hypoxia occurs in most solid tumors and is associated with aggressive disease and therapy resistance. Widespread changes in gene expression play a critical role in the biological response to hypoxia. However, most research has focused on hypoxia-inducible genes as opposed to those that are decreased in hypoxia. We demonstrate that chromatin accessibility is decreased in hypoxia, predominantly at gene promoters and specific pathways are impacted including DNA repair, splicing, and the R-loop interactome. One of the genes with decreased chromatin accessibility in hypoxia was DDX5, encoding the RNA helicase, DDX5, which showed reduced expression in various cancer cell lines in hypoxic conditions, tumor xenografts, and in patient samples with hypoxic tumors. Most interestingly, we found that when DDX5 is rescued in hypoxia, replication stress and R-loop levels accumulate further, demonstrating that hypoxia-mediated repression of DDX5 restricts R-loop accumulation. Together these data support the hypothesis that a critical part of the biological response to hypoxia is the repression of multiple R-loop processing factors; however, as shown for DDX5, their role is specific and distinct.

| S-EPMC10323886 | biostudies-literature

Nfib Promotes Metastasis through a Widespread Increase in Chromatin Accessibility.

Project description:Metastases are the main cause of cancer deaths, but the mechanisms underlying metastatic progression remain poorly understood. We isolated pure populations of cancer cells from primary tumors and metastases from a genetically engineered mouse model of human small cell lung cancer (SCLC) to investigate the mechanisms that drive the metastatic spread of this lethal cancer. Genome-wide characterization of chromatin accessibility revealed the opening of large numbers of distal regulatory elements across the genome during metastatic progression. These changes correlate with copy number amplification of the Nfib locus, and differentially accessible sites were highly enriched for Nfib transcription factor binding sites. Nfib is necessary and sufficient to increase chromatin accessibility at a large subset of the intergenic regions. Nfib promotes pro-metastatic neuronal gene expression programs and drives the metastatic ability of SCLC cells. The identification of widespread chromatin changes during SCLC progression reveals an unexpected global reprogramming during metastatic progression.

| S-EPMC5004630 | biostudies-literature

Transcriptional regulation mediated by H2A.Z via ANP32e-dependent inhibition of protein phosphatase 2A.

Project description:The mechanisms that regulate H2A.Z and its requirement for transcription in differentiated mammalian cells remains ambiguous. In this study, we identified the interaction between the C-terminus of ANP32e and N-terminus of H2A.Z in a yeast two-hybrid screen. Knockdown of ANP32e resulted in proteasomal degradation and nuclear depletion of H2A.Z or of a chimeric green florescence protein fused to its N-terminus. This effect was reversed by inhibition of protein phosphatase 2A (PP2A) and, conversely, reproduced by overexpression of its catalytic subunit. Accordingly, knockdown of ANP32e inhibited phosphorylation of H2A.Z, whereas a mutation of serine-9 proved its requirement for both the protein's stability and nuclear localization, as did knockdown of the nuclear mitogen and stress-induced kinase 1. Moreover, ANP32e's knockdown also revealed its differential requirement for cell signaling and gene expression, whereas, genome-wide binding analysis confirmed its co-localization with H2A.Z at transcription start sites, as well as, gene bodies of inducible and tissue-specific genes. The data also suggest that H2A.Z restricts transcription, which is moderated by ANP32e at the promoter and gene bodies of expressed genes. Thus, ANP32e, through inhibition of PP2A, is required for nucleosomal inclusion of H2A.Z and the regulation of gene expression.

| S-EPMC6053077 | biostudies-literature

Coactivator-Dependent Oscillation of Chromatin Accessibility Dictates Circadian Gene Amplitude through REV-ERB Loading

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-12-07 | E-GEOD-67860 | biostudies-arrayexpress