Thrap3 promotes R-loop resolution via interaction with methylated DDX5

Exp Mol Med. 2021 Oct;53(10):1602-1611. doi: 10.1038/s12276-021-00689-6. Epub 2021 Oct 25.

Abstract

Transcription-replication conflicts lead to DNA damage and genomic instability, which are closely related to human diseases. A major source of these conflicts is the formation of R-loops, which consist of an RNA-DNA hybrid and a displaced single-stranded DNA. Although these structures have been studied, many aspects of R-loop biology and R-loop-mediated genome instability remain unclear. Here, we demonstrate that thyroid hormone receptor-associated protein 3 (Thrap3) plays a critical role in regulating R-loop resolution. In cancer cells, Thrap3 interacts with DEAD-box helicase 5 (DDX5) and localizes to R-loops. Arginine-mediated methylation of DDX5 is required for its interaction with Thrap3, and the Thrap3-DDX5 axis induces the recruitment of 5'-3' exoribonuclease 2 (XRN2) into R-loops. Loss of Thrap3 increases R-loop accumulation and DNA damage. These findings suggest that Thrap3 mediates resistance to cell death by preventing R-loop accumulation in cancer cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • DEAD-box RNA Helicases / genetics
  • DEAD-box RNA Helicases / metabolism
  • DNA / genetics
  • DNA-Binding Proteins / metabolism
  • Genomic Instability
  • Humans
  • R-Loop Structures*
  • RNA
  • Transcription Factors* / genetics

Substances

  • DNA-Binding Proteins
  • THRAP3 protein, human
  • Transcription Factors
  • RNA
  • DNA
  • Ddx5 protein, human
  • DEAD-box RNA Helicases