The Experts below are selected from a list of 470232 Experts worldwide ranked by ideXlab platform

Luyuan Chang - One of the best experts on this subject based on the ideXlab platform.

  • histone variants h2a z and h3 3 coordinately regulate prc2 dependent h3k27me3 deposition and Gene Expression Regulation in mes cells
    BMC Biology, 2018
    Co-Authors: Yan Wang, Haizhen Long, Liping Dong, Michel Wassef, Baowen Zhuo, Jicheng Zhao, Min Wang, Cuifang Liu, Zengqi Wen, Luyuan Chang
    Abstract:

    Background The hierarchical organization of eukaryotic chromatin plays a central role in Gene Regulation, by controlling the extent to which the transcription machinery can access DNA. The histone variants H3.3 and H2A.Z have recently been identified as key regulatory players in this process, but the underlying molecular mechanisms by which they permit or restrict Gene Expression remain unclear. Here, we investigated the regulatory function of H3.3 and H2A.Z on chromatin dynamics and Polycomb-mediated Gene silencing.

  • histone variants h2a z and h3 3 coordinately regulate prc2 dependent h3k27me3 deposition and Gene Expression Regulation in mes cells
    BMC Biology, 2018
    Co-Authors: Yan Wang, Haizhen Long, Liping Dong, Michel Wassef, Baowen Zhuo, Jicheng Zhao, Min Wang, Cuifang Liu, Zengqi Wen, Luyuan Chang
    Abstract:

    The hierarchical organization of eukaryotic chromatin plays a central role in Gene Regulation, by controlling the extent to which the transcription machinery can access DNA. The histone variants H3.3 and H2A.Z have recently been identified as key regulatory players in this process, but the underlying molecular mechanisms by which they permit or restrict Gene Expression remain unclear. Here, we investigated the regulatory function of H3.3 and H2A.Z on chromatin dynamics and Polycomb-mediated Gene silencing. Our ChIP-seq analysis reveals that in mouse embryonic stem (mES) cells, H3K27me3 enrichment correlates strongly with H2A.Z. We further demonstrate that H2A.Z promotes PRC2 activity on H3K27 methylation through facilitating chromatin compaction both in vitro and in mES cells. In contrast, PRC2 activity is counteracted by H3.3 through impairing chromatin compaction. However, a subset of H3.3 may positively regulate PRC2-dependent H3K27 methylation via coordinating depositions of H2A.Z to developmental and signaling Genes in mES cells. Using all-trans retinoic acid (tRA)-induced Gene as a model, we show that the dynamic deposition of H2A.Z and H3.3 coordinately regulates the PRC2-dependent H3K27 methylation by modulating local chromatin structure at the promoter region during the process of turning Genes off. Our study provides key insights into the mechanism of how histone variants H3.3 and H2A.Z function coordinately to finely tune the PRC2 enzymatic activity during Gene silencing, through promoting or impairing chromosome compaction respectively.

Yan Wang - One of the best experts on this subject based on the ideXlab platform.

  • histone variants h2a z and h3 3 coordinately regulate prc2 dependent h3k27me3 deposition and Gene Expression Regulation in mes cells
    BMC Biology, 2018
    Co-Authors: Yan Wang, Haizhen Long, Liping Dong, Michel Wassef, Baowen Zhuo, Jicheng Zhao, Min Wang, Cuifang Liu, Zengqi Wen, Luyuan Chang
    Abstract:

    Background The hierarchical organization of eukaryotic chromatin plays a central role in Gene Regulation, by controlling the extent to which the transcription machinery can access DNA. The histone variants H3.3 and H2A.Z have recently been identified as key regulatory players in this process, but the underlying molecular mechanisms by which they permit or restrict Gene Expression remain unclear. Here, we investigated the regulatory function of H3.3 and H2A.Z on chromatin dynamics and Polycomb-mediated Gene silencing.

  • histone variants h2a z and h3 3 coordinately regulate prc2 dependent h3k27me3 deposition and Gene Expression Regulation in mes cells
    BMC Biology, 2018
    Co-Authors: Yan Wang, Haizhen Long, Liping Dong, Michel Wassef, Baowen Zhuo, Jicheng Zhao, Min Wang, Cuifang Liu, Zengqi Wen, Luyuan Chang
    Abstract:

    The hierarchical organization of eukaryotic chromatin plays a central role in Gene Regulation, by controlling the extent to which the transcription machinery can access DNA. The histone variants H3.3 and H2A.Z have recently been identified as key regulatory players in this process, but the underlying molecular mechanisms by which they permit or restrict Gene Expression remain unclear. Here, we investigated the regulatory function of H3.3 and H2A.Z on chromatin dynamics and Polycomb-mediated Gene silencing. Our ChIP-seq analysis reveals that in mouse embryonic stem (mES) cells, H3K27me3 enrichment correlates strongly with H2A.Z. We further demonstrate that H2A.Z promotes PRC2 activity on H3K27 methylation through facilitating chromatin compaction both in vitro and in mES cells. In contrast, PRC2 activity is counteracted by H3.3 through impairing chromatin compaction. However, a subset of H3.3 may positively regulate PRC2-dependent H3K27 methylation via coordinating depositions of H2A.Z to developmental and signaling Genes in mES cells. Using all-trans retinoic acid (tRA)-induced Gene as a model, we show that the dynamic deposition of H2A.Z and H3.3 coordinately regulates the PRC2-dependent H3K27 methylation by modulating local chromatin structure at the promoter region during the process of turning Genes off. Our study provides key insights into the mechanism of how histone variants H3.3 and H2A.Z function coordinately to finely tune the PRC2 enzymatic activity during Gene silencing, through promoting or impairing chromosome compaction respectively.

Alexandra Grubman - One of the best experts on this subject based on the ideXlab platform.

  • a single cell atlas of entorhinal cortex from individuals with alzheimer s disease reveals cell type specific Gene Expression Regulation
    Nature Neuroscience, 2019
    Co-Authors: Xin Yi Choo, Alexandra Grubman, Gabriel Chew, John F Ouyang, Guizhi Sun, Catriona Mclean
    Abstract:

    There is currently little information available about how individual cell types contribute to Alzheimer’s disease. Here we applied single-nucleus RNA sequencing to entorhinal cortex samples from control and Alzheimer’s disease brains (n = 6 per group), yielding a total of 13,214 high-quality nuclei. We detail cell-type-specific Gene Expression patterns, unveiling how transcriptional changes in specific cell subpopulations are associated with Alzheimer’s disease. We report that the Alzheimer’s disease risk Gene APOE is specifically repressed in Alzheimer’s disease oligodendrocyte progenitor cells and astrocyte subpopulations and upregulated in an Alzheimer’s disease-specific microglial subopulation. Integrating transcription factor regulatory modules with Alzheimer’s disease risk loci revealed drivers of cell-type-specific state transitions towards Alzheimer’s disease. For example, transcription factor EB, a master regulator of lysosomal function, regulates multiple disease Genes in a specific Alzheimer’s disease astrocyte subpopulation. These results provide insights into the coordinated control of Alzheimer’s disease risk Genes and their cell-type-specific contribution to disease susceptibility. These results are available at http://adsn.ddnetbio.com. Grubman et al. Generated a single-cell transcriptomic atlas of the entorhinal cortex from patients with Alzheimer’s disease and identified transcription factor networks predicted to control disease progression in a cell-subtype-specific way.

Zengqi Wen - One of the best experts on this subject based on the ideXlab platform.

  • histone variants h2a z and h3 3 coordinately regulate prc2 dependent h3k27me3 deposition and Gene Expression Regulation in mes cells
    BMC Biology, 2018
    Co-Authors: Yan Wang, Haizhen Long, Liping Dong, Michel Wassef, Baowen Zhuo, Jicheng Zhao, Min Wang, Cuifang Liu, Zengqi Wen, Luyuan Chang
    Abstract:

    Background The hierarchical organization of eukaryotic chromatin plays a central role in Gene Regulation, by controlling the extent to which the transcription machinery can access DNA. The histone variants H3.3 and H2A.Z have recently been identified as key regulatory players in this process, but the underlying molecular mechanisms by which they permit or restrict Gene Expression remain unclear. Here, we investigated the regulatory function of H3.3 and H2A.Z on chromatin dynamics and Polycomb-mediated Gene silencing.

  • histone variants h2a z and h3 3 coordinately regulate prc2 dependent h3k27me3 deposition and Gene Expression Regulation in mes cells
    BMC Biology, 2018
    Co-Authors: Yan Wang, Haizhen Long, Liping Dong, Michel Wassef, Baowen Zhuo, Jicheng Zhao, Min Wang, Cuifang Liu, Zengqi Wen, Luyuan Chang
    Abstract:

    The hierarchical organization of eukaryotic chromatin plays a central role in Gene Regulation, by controlling the extent to which the transcription machinery can access DNA. The histone variants H3.3 and H2A.Z have recently been identified as key regulatory players in this process, but the underlying molecular mechanisms by which they permit or restrict Gene Expression remain unclear. Here, we investigated the regulatory function of H3.3 and H2A.Z on chromatin dynamics and Polycomb-mediated Gene silencing. Our ChIP-seq analysis reveals that in mouse embryonic stem (mES) cells, H3K27me3 enrichment correlates strongly with H2A.Z. We further demonstrate that H2A.Z promotes PRC2 activity on H3K27 methylation through facilitating chromatin compaction both in vitro and in mES cells. In contrast, PRC2 activity is counteracted by H3.3 through impairing chromatin compaction. However, a subset of H3.3 may positively regulate PRC2-dependent H3K27 methylation via coordinating depositions of H2A.Z to developmental and signaling Genes in mES cells. Using all-trans retinoic acid (tRA)-induced Gene as a model, we show that the dynamic deposition of H2A.Z and H3.3 coordinately regulates the PRC2-dependent H3K27 methylation by modulating local chromatin structure at the promoter region during the process of turning Genes off. Our study provides key insights into the mechanism of how histone variants H3.3 and H2A.Z function coordinately to finely tune the PRC2 enzymatic activity during Gene silencing, through promoting or impairing chromosome compaction respectively.

Michel Wassef - One of the best experts on this subject based on the ideXlab platform.

  • histone variants h2a z and h3 3 coordinately regulate prc2 dependent h3k27me3 deposition and Gene Expression Regulation in mes cells
    BMC Biology, 2018
    Co-Authors: Yan Wang, Haizhen Long, Liping Dong, Michel Wassef, Baowen Zhuo, Jicheng Zhao, Min Wang, Cuifang Liu, Zengqi Wen, Luyuan Chang
    Abstract:

    Background The hierarchical organization of eukaryotic chromatin plays a central role in Gene Regulation, by controlling the extent to which the transcription machinery can access DNA. The histone variants H3.3 and H2A.Z have recently been identified as key regulatory players in this process, but the underlying molecular mechanisms by which they permit or restrict Gene Expression remain unclear. Here, we investigated the regulatory function of H3.3 and H2A.Z on chromatin dynamics and Polycomb-mediated Gene silencing.

  • histone variants h2a z and h3 3 coordinately regulate prc2 dependent h3k27me3 deposition and Gene Expression Regulation in mes cells
    BMC Biology, 2018
    Co-Authors: Yan Wang, Haizhen Long, Liping Dong, Michel Wassef, Baowen Zhuo, Jicheng Zhao, Min Wang, Cuifang Liu, Zengqi Wen, Luyuan Chang
    Abstract:

    The hierarchical organization of eukaryotic chromatin plays a central role in Gene Regulation, by controlling the extent to which the transcription machinery can access DNA. The histone variants H3.3 and H2A.Z have recently been identified as key regulatory players in this process, but the underlying molecular mechanisms by which they permit or restrict Gene Expression remain unclear. Here, we investigated the regulatory function of H3.3 and H2A.Z on chromatin dynamics and Polycomb-mediated Gene silencing. Our ChIP-seq analysis reveals that in mouse embryonic stem (mES) cells, H3K27me3 enrichment correlates strongly with H2A.Z. We further demonstrate that H2A.Z promotes PRC2 activity on H3K27 methylation through facilitating chromatin compaction both in vitro and in mES cells. In contrast, PRC2 activity is counteracted by H3.3 through impairing chromatin compaction. However, a subset of H3.3 may positively regulate PRC2-dependent H3K27 methylation via coordinating depositions of H2A.Z to developmental and signaling Genes in mES cells. Using all-trans retinoic acid (tRA)-induced Gene as a model, we show that the dynamic deposition of H2A.Z and H3.3 coordinately regulates the PRC2-dependent H3K27 methylation by modulating local chromatin structure at the promoter region during the process of turning Genes off. Our study provides key insights into the mechanism of how histone variants H3.3 and H2A.Z function coordinately to finely tune the PRC2 enzymatic activity during Gene silencing, through promoting or impairing chromosome compaction respectively.