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Templated insertions-DNA repair gets acrobatic.

Susanna Stroik1, Adam J Luthman2, Dale A Ramsden1,2,3

  • 1Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.

Environmental and Molecular Mutagenesis
|July 13, 2023
PubMed
Summary
This summary is machine-generated.

DNA double-strand break repair via polymerase theta (Polθ) can cause deletions and insertions. This study identifies a new "strand switching" insertion mechanism, contributing to diseases like cancer.

Keywords:
DNA double‐strand break repairTMEJcancerpolymerase theta

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Area of Science:

  • Molecular Biology
  • Genetics
  • Genomics

Background:

  • DNA double-strand breaks (DSBs) are repaired through various mechanisms, including theta-mediated end joining (TMEJ).
  • TMEJ is known to cause deletions via microhomology (MH) alignment.
  • TMEJ also possesses a templated insertion capability, less understood and linked to both deletions and insertions.

Purpose of the Study:

  • To investigate the mechanisms of polymerase theta (Polθ)-mediated templated insertions.
  • To characterize a newly identified class of Polθ-dependent insertions termed 'strand switching'.

Main Methods:

  • Analysis of DNA repair pathways, specifically focusing on polymerase theta.
  • Identification and characterization of direct, inverse, and strand switching templated insertions across multiple species and loci.

Main Results:

  • Polymerase theta mediates templated insertions through a multi-step synthesis process.
  • A novel class of templated insertions, 'strand switching,' was identified and observed at significant frequencies.
  • These Polθ-dependent insertions are frequently found in cancer genomes and repeat expansion disorders.

Conclusions:

  • Polymerase theta-mediated templated insertions, including the newly identified strand switching class, contribute to mutagenesis.
  • These mechanisms are implicated in the pathogenesis of diseases such as cancer and repeat expansion disorders.
  • Understanding Polθ insertion mechanisms offers potential for novel therapeutic strategies.