Scholarlink

<p>The three-dimensional (3D) chromatin structure of Epstein–Barr virus (EBV) within host cells and the underlying mechanisms of chromatin interaction and gene regulation, particularly those involving EBV’s noncoding RNAs (ncRNAs), have remained incompletely characterized. In this study, we employed state-of-the-art techniques of 3D genome mapping, including protein-associated chromatin interaction analysis with paired-end tag sequencing (ChIA-PET), RNA-associated chromatin interaction technique (RDD), and super-resolution microscopy, to delineate the spatial architecture of EBV in human lymphoblastoid cells. We systematically analyzed EBV-to-EBV (E–E), EBV-to-host (E–H), and host-to-host (H–H) interactions linked to host proteins and EBV RNAs. Our findings reveal that EBV utilizes host CCCTC-binding factor (CTCF) and RNA polymerase II (RNAPII) to form distinct chromatin contact domains (CCDs) and RNAPII-associated interaction domains (RAIDs). The anchors of these chromatin domains serve as platforms for extensive interactions with host chromatin, thus modulating host gene expression. Notably, EBV ncRNAs, especially Epstein–Barr-encoded RNAs (EBERs), target and interact with less accessible regions of host chromatin to repress a subset of genes via the inhibition of RNAPII-associated chromatin loops. This process involves the cofactor nucleolin (NCL) and its RNA recognition motifs, and depletion of either NCL or EBERs alters expression of genes crucial for host infection control, immune response, and cell cycle regulation. These findings unveil a sophisticated interplay between EBV and host chromatin.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Landscape of the Epstein-Barr virus-host chromatin interactome and gene regulation

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年5月27日

查看全文
  • Simon Zhongyuan Tian,
  • Yang Yang,
  • Duo Ning,
  • Ting Yu,
  • Tong Gao,
  • Yuqing Deng,
  • Ke Fang,
  • Yewen Xu,
  • Kai Jing,
  • Guangyu Huang,
  • Gengzhan Chen,
  • Pengfei Yin,
  • Yiming Li,
  • Fuxing Zeng,
  • Ruilin Tian,
  • Meizhen Zheng

摘要

The three-dimensional (3D) chromatin structure of Epstein–Barr virus (EBV) within host cells and the underlying mechanisms of chromatin interaction and gene regulation, particularly those involving EBV’s noncoding RNAs (ncRNAs), have remained incompletely characterized. In this study, we employed state-of-the-art techniques of 3D genome mapping, including protein-associated chromatin interaction analysis with paired-end tag sequencing (ChIA-PET), RNA-associated chromatin interaction technique (RDD), and super-resolution microscopy, to delineate the spatial architecture of EBV in human lymphoblastoid cells. We systematically analyzed EBV-to-EBV (E–E), EBV-to-host (E–H), and host-to-host (H–H) interactions linked to host proteins and EBV RNAs. Our findings reveal that EBV utilizes host CCCTC-binding factor (CTCF) and RNA polymerase II (RNAPII) to form distinct chromatin contact domains (CCDs) and RNAPII-associated interaction domains (RAIDs). The anchors of these chromatin domains serve as platforms for extensive interactions with host chromatin, thus modulating host gene expression. Notably, EBV ncRNAs, especially Epstein–Barr-encoded RNAs (EBERs), target and interact with less accessible regions of host chromatin to repress a subset of genes via the inhibition of RNAPII-associated chromatin loops. This process involves the cofactor nucleolin (NCL) and its RNA recognition motifs, and depletion of either NCL or EBERs alters expression of genes crucial for host infection control, immune response, and cell cycle regulation. These findings unveil a sophisticated interplay between EBV and host chromatin.