Genome-wide Chromatin Accessibility is Restricted by ANP32E [CUT&Tag]
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ABSTRACT:
PROVIDER: PRJNA650548 | ENA |
REPOSITORIES: ENA
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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.
2020-09-08 | GSE155647 | GEO
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.
2020-09-08 | GSE145703 | GEO
Project description:Genome-wide Chromatin Accessibility is Restricted by ANP32E [ATAC-seq]
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Project description:We report the enrichment of ANP32E in MCF-7 cells assayed with CUT&Tag sequencing.
2021-11-16 | GSE188942 | GEO
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
Project description:To map the chromatin binding sites for SMC1 in OE19 cells, we performed CUT&TAG.
2024-09-25 | E-MTAB-14090 | biostudies-arrayexpress
Project description:To map the chromatin binding sites for various factors in OE19 cells, we performed CUT&TAG.
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Project description:We present spatially resolved high-spatial-resolution genome-wide co-mapping of epigenome and transcriptome by simultaneously profiling of chromatin accessibility and gene expression (spatial-ATAC-RNA-seq), as well as histone modification and gene expression (spatial-CUT&Tag-RNA-seq) on the same tissue section at cellular level by combining the microfluidic deterministic barcoding strategy in DBiT-seq and the chemistry used in ATAC-seq/CUT&Tag.
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Project description:We developed scNanoSeq-CUT&Tag, a streamlined method by adapting a modified CUT&Tag protocol to Oxford Nanopore sequencing platform for efficient chromatin modification profiling at single-cell resolution. We firstly tested the performance of scNanoSeq-CUT&Tag on six human cell lines: K562, 293T, GM12878, HG002, H9, HFF1 and adult mouse blood cells, it showed that scNanoSeq-CUT&Tag can accurately distinguish different cell types in vitro and in vivo. Moreover, scNanoSeq-CUT&Tag enables to effectively map the allele-specific epigenomic modifications in the human genome andallows to analyze co-occupancy of histone modifications. Taking advantage of long-read sequencing,scNanoSeq-CUT&Tag can sensitively detect epigenomic state of repetitive elements. In addition, by applying scNanoSeq-CUT&Tag to testicular cells of adult mouse B6D2F1, we demonstrated that scNanoSeq-CUT&Tag maps dynamic epigenetic state changes during mouse spermatogenesis. Finally, we exploited the epigenetic changes of human leukemia cell line K562 during DNA demethylation, it showed that NanoSeq-CUT&Tag can capture H3K27ac signals changes along DNA demethylation. Overall, we prove that scNanoSeq-CUT&Tag is a valuable tool for efficiently probing chromatin state changes within individual cells.
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