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The transcriptional coactivator RUVBL2 regulates Pol II clustering with diverse transcription factors

  • Hui Wang
  • , Boyuan Li
  • , Linyu Zuo
  • , Bo Wang
  • , Yan Yan
  • , Kai Tian
  • , Rong Zhou
  • , Chenlu Wang
  • , Xizi Chen
  • , Yongpeng Jiang
  • , Haonan Zheng
  • , Fangfei Qin
  • , Bin Zhang
  • , Yang Yu
  • , Chao Pei Liu
  • , Yanhui Xu
  • , Juntao Gao
  • , Zhi Qi
  • , Wulan Deng
  • , Xiong Ji*
  • *此作品的通讯作者
  • Key Laboratory of Cell Proliferation and Differentiation of the Ministry of Education
  • Peking University
  • Department of Pathogenic Biology
  • Chengdu Medical College
  • Center for Quantitative Biology
  • Biomedical Pioneering Innovation Center (BIOPIC)
  • Tsinghua University
  • Center for Synthetic and Systems Biology
  • Institutes of Biomedical Sciences
  • Fudan University
  • Synthetic and Functional Biomolecules Center
  • Departments of Pathology and Laboratory Medicine
  • University of Rochester
  • Key Laboratory of RNA Biology
  • CAS - Institute of Biophysics
  • National Laboratory of Biomacromolecules

科研成果: 期刊稿件 › 文章 › 同行评审

摘要

RNA polymerase II (Pol II) apparatuses are compartmentalized into transcriptional clusters. Whether protein factors control these clusters remains unknown. In this study, we find that the ATPase-associated with diverse cellular activities (AAA +) ATPase RUVBL2 co-occupies promoters with Pol II and various transcription factors. RUVBL2 interacts with unphosphorylated Pol II in chromatin to promote RPB1 carboxy-terminal domain (CTD) clustering and transcription initiation. Rapid depletion of RUVBL2 leads to a decrease in the number of Pol II clusters and inhibits nascent RNA synthesis, and tethering RUVBL2 to an active promoter enhances Pol II clustering at the promoter. We also identify target genes that are directly linked to the RUVBL2-Pol II axis. Many of these genes are hallmarks of cancers and encode proteins with diverse cellular functions. Our results demonstrate an emerging activity for RUVBL2 in regulating Pol II cluster formation in the nucleus.

源语言英语
期刊论文编号5703
期刊Nature Communications
卷13
期1
DOI
出版状态已出版 - 12月 2022
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