MYOD Regulation of 3D Chromatin Structure

3D 染色质结构的 MYOD 调节

基本信息

项目摘要

PROJECT SUMMARY This proposal aims at providing mechanistic insights into MYOD regulation of the high-order chromatin interactions that define the 3D nuclear architecture of skeletal muscle cells, by capitalizing on the unprecedented availability of high-resolution matrices of the genomic interactions induced by MYOD during skeletal myogenesis from our preliminary studies. This study will fill a critical gap of basic knowledge in the control of transcription and muscle stem cell biology, by exploring a higher level of complexity in the regulation of gene expression in muscle satellite cells introduced by the spatial dimension. The Specific Aims are: Aim 1 Molecular analysis of MYOD-directed regulation of 3D chromatin structure in muscle progenitors. 1a To determine the contribution of specific MYOD domains to structural and functional alterations of high-order chromatin interactions that regulate gene expression. We will monitor the effect of MYOD mutants on 3D chromatin structure and transcriptional output at specific loci. 1b To determine the role of co-factors in MYOD- directed rewiring of chromatin interactions that regulate gene expression. We will investigate the role of architectural proteins (CTCF and cohesin) as well as specific components of the chromatin-remodeling complex and the transcriptional machinery - including BAF60C, Polymerase II (PolII), TAF3, Bromodomain and Extra-Terminal Domain (BET) proteins - in MYOD-directed reconfiguration of chromatin interactions within specific nuclear topological domains. 1c To investigate MYOD-directed control of high-order chromatin interactions in satellite cells. We will determine the role of MYOD and co-factors on regulation of 3D chromatin interactome and transcriptional output in satellite cells isolated from a mouse model of conditional genetic ablation of MyoD. Aim 2 MYOD-directed regulation of 3D chromatin structure for signal-dependent control of gene expression 2a. To functionally challenge MYOD-regulated cis-regulatory elements for signal- regulated gene expression. We will exploit Cas9-based genome editing, RNAi-based knockdown and pharmacological targeting of key epigenetic events to interrogate the dynamics of enhancer activation and chromatin interactions in response to extrinsic signals in MYOD-converted IMR90 fibroblasts. 2b To investigate MYOD-regulated cis-regulatory elements for satellite cell response to regeneration cues. We will use mouse models of satellite cell conditional genetic ablation of MyoD or the signal-responsive component of the SWI/SNF chromatin-remodeling complex BAF60C, to investigate the functional relationship between MYOD, chromatin remodeling and changes in chromatin interactions for signal-regulated gene expression. Data from this study will provide fundamental insights into the spatial control of eukaryotic transcription and satellite cell biology that will favor the transition in regenerative medicine from current therapeutic strategies affecting global gene expression to tailored approaches, based on genome editing techniques, toward a selective targeting of individual genes in satellite cells exposed to pathogenic cues from diseased muscles.
项目总结

项目成果

期刊论文数量(1)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
MyoD induces ARTD1 and nucleoplasmic poly-ADP-ribosylation during fibroblast to myoblast transdifferentiation.
  • DOI:
    10.1016/j.isci.2021.102432
  • 发表时间:
    2021-05-21
  • 期刊:
  • 影响因子:
    5.8
  • 作者:
    Bisceglie L;Hopp AK;Gunasekera K;Wright RH;Le Dily F;Vidal E;Dall'Agnese A;Caputo L;Nicoletti C;Puri PL;Beato M;Hottiger MO
  • 通讯作者:
    Hottiger MO
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Pier Lorenzo Puri其他文献

Nitric Oxide and Histone Acetylation—Shaping Craniofacial Development
  • DOI:
    10.1016/j.chembiol.2014.05.002
  • 发表时间:
    2014-05-22
  • 期刊:
  • 影响因子:
  • 作者:
    Libera Berghella;Pier Lorenzo Puri
  • 通讯作者:
    Pier Lorenzo Puri
HDAC inhibitors as pharmacological treatment for Duchenne muscular dystrophy: a discovery journey from bench to patients
组蛋白去乙酰化酶抑制剂作为杜氏肌营养不良症的药物治疗方法:从实验室到患者的探索之旅
  • DOI:
    10.1016/j.molmed.2024.01.007
  • 发表时间:
    2024-03-01
  • 期刊:
  • 影响因子:
    13.800
  • 作者:
    Chiara Mozzetta;Vittorio Sartorelli;Pier Lorenzo Puri
  • 通讯作者:
    Pier Lorenzo Puri
RETRACTED ARTICLE: Association of Ataxia Telangiectasia Mutated (ATM) gene mutation/deletion with Rhabdomyosarcoma
  • DOI:
    10.1186/1476-4598-2-2
  • 发表时间:
    2003-01-03
  • 期刊:
  • 影响因子:
    33.900
  • 作者:
    Peilin Zhang;Kunjan S Bhakta;Pier Lorenzo Puri;Robert O Newbury;James R Feramisco;Jean Y Wang
  • 通讯作者:
    Jean Y Wang
Nuclear factor-kappaB and cAMP response element binding protein mediate opposite transcriptional effects on the Flk-1/KDR gene promoter.
核因子-kappaB 和 cAMP 反应元件结合蛋白介导 Flk-1/KDR 基因启动子上相反的转录作用。
  • DOI:
  • 发表时间:
    2000
  • 期刊:
  • 影响因子:
    20.1
  • 作者:
    B. Illi;Pier Lorenzo Puri;Liliana Morgante;M. Capogrossi;C. Gaetano
  • 通讯作者:
    C. Gaetano
Retraction Note: Association of Ataxia Telangiectasia Mutated (ATM) Gene Mutation/Deletion with Rhabdomyosarcoma – retraction
  • DOI:
    10.1186/1476-4598-2-17
  • 发表时间:
    2003-01-01
  • 期刊:
  • 影响因子:
    33.900
  • 作者:
    Peilin Zhang;Kunjan S Bhakta;Pier Lorenzo Puri;Robert O Newbury;James R Feramisco;Jean Y Wang
  • 通讯作者:
    Jean Y Wang

Pier Lorenzo Puri的其他文献

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{{ truncateString('Pier Lorenzo Puri', 18)}}的其他基金

Role of Fbxw7-Mediated Proteasomal Degradation in Myofibers in Determining Muscle Stem Cell Pool Size
Fbxw7 介导的肌纤维蛋白酶体降解在确定肌肉干细胞库大小中的作用
  • 批准号:
    10438706
  • 财政年份:
    2020
  • 资助金额:
    $ 39万
  • 项目类别:
Role of Fbxw7-Mediated Proteasomal Degradation in Myofibers in Determining Muscle Stem Cell Pool Size
Fbxw7 介导的肌纤维蛋白酶体降解在确定肌肉干细胞库大小中的作用
  • 批准号:
    10206003
  • 财政年份:
    2020
  • 资助金额:
    $ 39万
  • 项目类别:
MYOD Regulation of 3D Chromatin Structure
3D 染色质结构的 MYOD 调节
  • 批准号:
    9974548
  • 财政年份:
    2019
  • 资助金额:
    $ 39万
  • 项目类别:
Denervation activated super-enhancers of pathogenic IL6-STAT3 feedforward loop in FAPs
FAP 中致病性 IL6-STAT3 前馈环的去神经激活超级增强子
  • 批准号:
    10177874
  • 财政年份:
    2019
  • 资助金额:
    $ 39万
  • 项目类别:
Denervation activated super-enhancers of pathogenic IL6-STAT3 feedforward loop in FAPs
FAP 中致病性 IL6-STAT3 前馈环的去神经激活超级增强子
  • 批准号:
    10410466
  • 财政年份:
    2019
  • 资助金额:
    $ 39万
  • 项目类别:
Denervation activated super-enhancers of pathogenic IL6-STAT3 feedforward loop in FAPs
FAP 中致病性 IL6-STAT3 前馈环的去神经激活超级增强子
  • 批准号:
    10634547
  • 财政年份:
    2019
  • 资助金额:
    $ 39万
  • 项目类别:
Dystrophin signaling and the epigenetic landscape of human iPSC-derived muscles
肌营养不良蛋白信号传导和人类 iPSC 衍生肌肉的表观遗传景观
  • 批准号:
    8774130
  • 财政年份:
    2009
  • 资助金额:
    $ 39万
  • 项目类别:
Dystrophin signaling and the epigenetic landscape of human iPSC-derived muscles
肌营养不良蛋白信号传导和人类 iPSC 衍生肌肉的表观遗传景观
  • 批准号:
    9330676
  • 财政年份:
    2009
  • 资助金额:
    $ 39万
  • 项目类别:
Dystrophin signaling and the epigenetic landscape of human iPSC-derived muscles
肌营养不良蛋白信号传导和人类 iPSC 衍生肌肉的表观遗传景观
  • 批准号:
    8897264
  • 财政年份:
    2009
  • 资助金额:
    $ 39万
  • 项目类别:
Pathogenic Alterations of the 3D Epigenetic Landscape in Dystrophin-Deficient Skeletal Muscles and Reversal by Dystrophin Re-Expression
肌营养不良蛋白缺陷骨骼肌 3D 表观遗传景观的致病性改变以及肌营养不良蛋白重新表达的逆转
  • 批准号:
    10631048
  • 财政年份:
    2009
  • 资助金额:
    $ 39万
  • 项目类别:

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