Scholarlink

Background <p>CTCF, a highly studied transcription factor, is essential for chromatin interaction maintenance. Several independent studies report that CTCF interacts with RNAs in vitro and in cells. Yet continuous debates about the authenticity of the RNA-binding affinity of CTCF and its biological role remain in large part due to limited research techniques available, such as CLIP-seq.</p> Result <p>Here, we investigate RNA’s role in CTCF’s transcription factor function through its chromatin occupancy. To systematically explore whether RNAs affect CTCF’s ability to bind DNA, we perturb CTCF-RNA interactions by three independent approaches and examine CTCF genome occupancy by ChIP-seq. Although RNase A and triptolide treatment each affect a certain number of CTCF-binding peaks, few peaks overlap between treatment groups indicating the effect of RNA in regulating CTCF’s DNA binding affinity is variable between loci. In addition, limited transcriptional or chromatin accessibility changes occur between cells expressing wild-type CTCF or CTCF lacking the RNA binding region.</p> Conclusion <p>Our data provide a complementary approach and in silico evidence to consider the significance of RNA affecting CTCF’s DNA binding affinity globally.</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

Deciphering the role of RNA in regulating CTCF’s DNA binding affinity in leukemia cells

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年5月12日

查看全文
  • Judith Hyle,
  • Wenjie Qi,
  • Mohamed Nadhir Djekidel,
  • Wojciech Rosikiewicz,
  • Beisi Xu,
  • Chunliang Li

摘要

Background

CTCF, a highly studied transcription factor, is essential for chromatin interaction maintenance. Several independent studies report that CTCF interacts with RNAs in vitro and in cells. Yet continuous debates about the authenticity of the RNA-binding affinity of CTCF and its biological role remain in large part due to limited research techniques available, such as CLIP-seq.

Result

Here, we investigate RNA’s role in CTCF’s transcription factor function through its chromatin occupancy. To systematically explore whether RNAs affect CTCF’s ability to bind DNA, we perturb CTCF-RNA interactions by three independent approaches and examine CTCF genome occupancy by ChIP-seq. Although RNase A and triptolide treatment each affect a certain number of CTCF-binding peaks, few peaks overlap between treatment groups indicating the effect of RNA in regulating CTCF’s DNA binding affinity is variable between loci. In addition, limited transcriptional or chromatin accessibility changes occur between cells expressing wild-type CTCF or CTCF lacking the RNA binding region.

Conclusion

Our data provide a complementary approach and in silico evidence to consider the significance of RNA affecting CTCF’s DNA binding affinity globally.