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Resolution of R-loops and transcription-replication conflicts by SETX-BRCA1-BARD1 complex.

Arijit Dutta1,2,3, Jae-Hoon Ji1,2, Shahrez Syed1,2

  • 1Department of Biochemistry and Structural Biology, University of Texas Health at San Antonio, San Antonio, TX, USA.

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|April 1, 2026
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Senataxin (SETX) and BRCA1-BARD1 resolve RNA-DNA hybrids (R-loops), preventing genome instability. This study reveals how their synergy maintains DNA integrity by resolving transcription-replication conflicts.

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Area of Science:

  • Molecular Biology
  • Genetics
  • Biochemistry

Background:

  • Senataxin (SETX) is an RNA-DNA helicase involved in genome maintenance.
  • BRCA1-BARD1 complex plays a role in DNA repair and transcription regulation.
  • Transcription-associated R-loops can lead to genomic instability if not resolved.

Purpose of the Study:

  • To elucidate the mechanism by which SETX and BRCA1-BARD1 cooperate to resolve R-loops.
  • To understand how this complex prevents transcription-replication conflicts and DNA damage.

Main Methods:

  • In vitro biochemical assays to study SETX and BRCA1-BARD1 interactions and R-loop unwinding.
  • Analysis of SETX phosphorylation and its effect on BRCA1 binding.
  • Cellular assays to assess R-loop accumulation, DNA breaks, and replication fork stalling in cells with SETX mutations.

Main Results:

  • SETX unwinds R-loops broadly; BRCA1-BARD1 binds R-loops and stimulates SETX activity.
  • BRCA1-BARD1 overcomes RAD52 inhibition of SETX.
  • SETX phosphorylation at Ser642 enhances BRCA1 interaction; SETX mutations cause R-loop accumulation and DNA damage.

Conclusions:

  • The synergistic action of SETX and BRCA1-BARD1 is crucial for efficient R-loop resolution.
  • This mechanism prevents transcription-replication conflicts, safeguarding genome integrity.
  • Phosphorylation of SETX at Ser642 is a key regulatory step for its interaction with BRCA1.