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Genome-wide Chromatin Accessibility is Restricted by ANP32E [CUT&Tag]

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE155647 | GEO | 2020/09/08

REPOSITORIES: GEO

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Genome-wide Chromatin Accessibility is Restricted by ANP32E [ATAC-seq]

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.

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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.

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Anp32e is a histone chaperone that removes H2A.Z from chromatin

Project description:We report a genome wide enrichment, redistribution and accumulation of H2A.Z at specific chromatin control regions, in particular at enhancers and insulators, in mouse embryonic fibroblasts depleted for Anp32e (MEFs Anp32e-/-). H2A.Z ChIP-seq in MEFs WT (+/+) or KO (-/-) for Anp32e.

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ANP32e binds histone H2A.Z in a cell cycle-dependent manner and regulates its protein stability in the cytoplasm

Project description:ANP32e, a chaperone of H2A.Z, is receiving increasing attention because of its link to cancer growth and progression. An unanswered question is whether ANP32e regulates H2A.Z dynamics during the cell cycle; if so, this could have clear implications for the proliferation of cancer cells. Using the human U2OS cancer cell line model system, we have confirmed that ANP32e regulates the growth of these cells. ANP32e preferentially interacts with H2A.Z during G1 phase of the cell cycle. Unexpectedly, however, ANP32e does not mediate the removal of H2A.Z from chromatin, is not a stable component of the p400 remodeling complex, and is not strongly associated with chromatin. Instead, most ANP32e is in the cytoplasm. Here, ANP32e preferentially interacts with H2A.Z in G1 phase in response to an increase in H2A.Z protein abundance and regulates its protein stability. This G1-specific interaction between ANP32e and H2A.Z is also observed in the nucleoplasm but is unrelated to any change in H2A.Z abundance. Collectively, these results challenge the idea that ANP32e is involved in regulating the abundance of H2A.Z in chromatin as part of a chromatin remodeling complex. Rather, we propose that ANP32e acts as a molecular chaperone that maintains the soluble pool of H2A.Z by regulating its protein stability and acting as a buffer in response to cell cycle-dependent changes in H2A.Z abundance.

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Anp32e is a histone chaperone that removes H2A.Z from chromatin

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The histone chaperone Anp32e regulates memory formation, transcription and dendritic morphogenesis by regulating steady-state H2A.Z binding in neurons

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Project description:Epigenetic regulation of chromatin states is crucial for proper gene expression programs and progression during development, but precise mechanisms by which epigenetic factors influence differentiation remain poorly understood. Here we find that the histone variant H2A.Z accumulates at Sox motif-containing promoters during zebrafish gastrulation while neighboring genes become transcriptionally active. These changes coincide with reduced expression of anp32e, the H2A.Z histone removal chaperone, suggesting that loss of Anp32e may lead to increases in H2A.Z binding during differentiation. Remarkably, genetic removal of Anp32e in embryos leads to H2A.Z accumulation prior to gastrulation and developmental genes become precociously active. Accordingly, H2A.Z accumulation occurs most extensively at Sox motif-associated genes, including many which are normally activated following gastrulation. Altogether, our results provide compelling evidence for a mechanism in which Anp32e preferentially restricts H2A.Z accumulation at Sox motifs to regulate the initial phases of developmental differentiation in zebrafish.

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ANP32E Restricts Widespread Chromatin Accessibility Through Regulation of H2A.Z

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

| PRJNA607979 | ENA

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 genes. The data also suggest that H2A.Z restricts transcription, which is moderated by ANP32e after induction of transcriptional activity of inducible and housekeeping genes vs. constitutively-expressed tissue-specific genes during cellular growth. Thus, ANP32e, through inhibition of PP2A, is required for nucleosomal inclusion of H2A.Z and the regulation of gene expression.

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Cell-Type-Specific Epigenetic Priming of Gene Expression in Nucleus Accumbens by Cocaine [ATAC-seq]

Project description:A hallmark of addiction is the ability of drugs of abuse to trigger relapse after periods of prolonged abstinence. Here, we describe a novel epigenetic mechanism whereby chronic cocaine exposure causes lasting chromatin and downstream transcriptional modifications in the nucleus accumbens (NAc), a critical brain region controlling motivation. We link prolonged withdrawal from cocaine to the depletion of the histone variant H2A.Z, coupled with increased genome accessibility and latent priming of gene transcription, in D1 dopamine receptor-expressing medium spiny neurons (D1 MSNs) that relate to aberrant gene expression upon drug relapse. The histone chaperone ANP32E removes H2A.Z from chromatin, and we demonstrate that D1 MSN-selective Anp32e knockdown prevents cocaine-induced H2A.Z depletion and blocks cocaine’s rewarding actions. By contrast, very different effects of cocaine exposure, withdrawal, and relapse were found for D2 MSNs. These findings establish histone variant exchange as an important mechanism and clinical target engaged by drugs of abuse to corrupt brain function and behavior.

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