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The ORFIUS complex regulates ORC2 localization at replication origins.

Zelei Yang1, Saie Mogre1, Ruiyang He1

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BRD1 suppresses replication stress in ovarian cancer by forming the ORFIUS complex, which regulates DNA replication origins. Dysregulation of this complex in high-grade serous ovarian cancer (HGSC) may drive tumor survival.

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Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genetics

Background:

  • High-grade serous ovarian cancer (HGSC) is characterized by high replication stress (RS) and impaired DNA damage responses.
  • Understanding the mechanisms that regulate DNA replication origins under stress is crucial for developing new cancer therapies.

Purpose of the Study:

  • To investigate the role of bromodomain-containing protein 1 (BRD1) in regulating replication origins during replication stress in HGSC.
  • To identify the protein complex involved in origin regulation under stress and its potential role in HGSC pathogenesis.

Main Methods:

  • Co-immunoprecipitation to identify protein interactions.
  • Immunofluorescence microscopy to assess protein localization at replication origins.
  • Cell-based assays to evaluate origin firing and DNA damage response.

Main Results:

  • BRD1 forms the ORigin FIring Under Stress (ORFIUS) complex with HBO1, BRCA1, and BARD1.
  • BRD1 and HBO1 support origin licensing protein ORC2 localization, promoting origin firing.
  • In HGSC cells, the ORFIUS complex is dysregulated, remaining associated with origins and unresponsive to stress signals, leading to increased origin firing despite DNA damage.

Conclusions:

  • BRD1 is a key component of the ORFIUS complex that suppresses replication stress by regulating DNA replication origins.
  • ORFIUS complex dysregulation in HGSC contributes to tumor cell survival by allowing continued replication and cell cycle progression under DNA damage.
  • The ORFIUS complex represents a potential therapeutic target for HGSC.