Crosstalk between TGF-β Signaling and Epigenome

来源 :TGF-β Signaling and Diseases Symposium(TGF-B信号转导与疾病专题研讨会) | 被引量 : 0次 | 上传用户:wangxun416
下载到本地 , 更方便阅读
声明 : 本文档内容版权归属内容提供方 , 如果您对本文有版权争议 , 可与客服联系进行内容授权或下架
论文部分内容阅读
Specific chromatin marks keep master regulators of differentiation silent yet poised for activation by extracellular signals.We report that nodal TGF-β signals use the poised histone mark H3K9me3 to trigger differentiation of mammalian embryonic stem cells.Nodal receptors induce the formation of companion Smad4-Smad2/3 and TRIM33-Smad2/3 complexes.The PHD-Bromo cassette of TRIM33 facilitates binding of TRIM33-Smad2/3 to H3K9me3 and H3K18ac on the promoters of mesendoderm regulators Gsc and Mixl1.The crystal structure of this cassette, bound to histone H3 peptides, illustrates that PHD recognizes K9me3, and Bromo binds an adjacent K18ac.The interaction between TRIM33-Smad2/3 and H3K9me3 displaces the chromatin-compacting factor HP1g, making nodal response elements accessible to Smad4-Smad2/3 for Pol Ⅱ recruitment.In turn,Smad4 increases K18 acetylation to augment TRIM33-Smad2/3 binding.Thus, nodal effectors use the H3K9me3 mark as a platform to switch master regulators of stem cell differentiation from the poised to the active state.
其他文献
会议
会议
主要内容·背景介绍·基线qAnti-HBc水平预测治疗应答-ADV-LdT-PEG-IFN-ETV·qAnti-HBc水平在自然史中的意义·研究展望目前抗HBV治疗指证是免疫活化期的HBV感染患者Trepo.C.
会议
During the late stage of cancer, TGF-β signaling pathway often enforces tumor metastatic behavior, by its immune tolerance function and its capacity to drive t
会议
以终为始弹棉花Garbage in,Garbage out 小成本VS大制作小成本:ALT的故事ALT的故事·纵向队列·有序随访·进出有序(来由影,去有踪)大制作:总体思路套娃总体思路:建设长期随
会议