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The CGG triplet repeat binding protein 1 counteracts R-loop induced transcription-replication stress.

Henning Ummethum1, Augusto C Murriello1, Marcel Werner1

  • 1Institute of Epigenetics and Stem Cells (IES), Helmholtz Munich, Feodor-Lynen-Strasse 21, Munich, 81377, Germany.

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Summary
This summary is machine-generated.

CGG triplet repeat binding protein 1 (CGGBP1) prevents transcription-replication conflicts at CGG repeats. Loss of CGGBP1 causes R-loop accumulation and transcription defects, highlighting its role in genome stability.

Keywords:
CGG Triplet Repeat Binding Protein 1CGG-trinucleotide RepeatsDDX41 RNA:DNA HelicaseR-loop StructureTranscription-Replication Conflicts

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Area of Science:

  • Molecular Biology
  • Genetics
  • Epigenetics

Background:

  • CGG triplet repeat binding protein 1 (CGGBP1) binds CGG repeats, but its role in transcription and replication is unclear.
  • Short CGG repeats in gene promoters can form R-loops, potentially disrupting cellular processes.

Purpose of the Study:

  • To investigate the function of CGGBP1 in regulating transcription and replication at CGG repeat sequences.
  • To identify CGGBP1's molecular partners and mechanisms in maintaining genome stability.

Main Methods:

  • Analysis of CGGBP1 binding to CGG repeats in human gene promoters.
  • Assessment of transcription, R-loop formation, and RNA polymerase II (RNAPII) activity in CGGBP1-depleted cells.
  • Identification of CGGBP1 interacting proteins using co-depletion experiments.

Main Results:

  • CGGBP1 binds to CGG repeats in promoters prone to R-loop formation.
  • Loss of CGGBP1 leads to deregulated transcription, R-loop accumulation, and transcription-replication conflicts (TRCs).
  • CGGBP1 recruits DDX41 and DHX15 helicases to resolve R-loops and prevent TRCs.

Conclusions:

  • Short CGG repeats are a source of genome-destabilizing secondary structures.
  • CGGBP1 and its interacting helicases are crucial for coordinating transcription and replication at CGG repeats.
  • Maintaining proper transcription-replication coordination is essential for genome stability.