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Related Experiment Video

Updated: Apr 9, 2026

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DNA Replication Errors Drive Genome-Wide Small Inverted Triplication Dynamics.

Yi Lei1, Yu Zhou1, Haitao Sun1

  • 1Department of Cancer Genetics and Epigenetics, Beckman Research Institute, City of Hope, Duarte, California, USA.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|April 7, 2026
PubMed
Summary
This summary is machine-generated.

Structural variants, like small inverted triplications (SITs), impact disease. Researchers found FEN1 protein is linked to SITs, uncovering mechanisms of their formation and elimination in DNA.

Keywords:
DNA replicationOkazaki fragment maturation (OFM)cancer genomicsflap endonuclease 1 (FEN1)small inverted triplication (SIT)

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Area of Science:

  • Genomics and Molecular Biology
  • Cancer Research
  • DNA Repair Mechanisms

Background:

  • Structural variants (SVs) significantly influence phenotype, diversity, and are implicated in human diseases.
  • Understanding the origins of SVs, particularly small inverted triplications (SITs), is crucial for disease research.
  • FEN1 (Flap Endonuclease 1) is a key enzyme in DNA replication and repair, potentially involved in genome instability.

Purpose of the Study:

  • To investigate the origination mechanisms of small inverted triplications (SITs) and their association with FEN1.
  • To characterize the structural features of novel SIT events identified in cancer genomes.
  • To explore the role of FEN1 in SIT formation and develop tools for SIT annotation.

Main Methods:

  • Analysis of 1,340 cancer genomes to identify and annotate 4,608 novel small inverted triplication (SIT) events.
  • Long-read sequencing and development of PacBioR tool for SIT annotation in yeast FEN1 mutant cells.
  • In vitro studies using E. coli system to investigate SIT elimination mechanisms via DNA polymerase slippage.

Main Results:

  • A strong association was found between FEN1 and the incidence of SIT events.
  • SITs were characterized as smaller DUP/IN/DUP structures (average 148/160/148 bp) with specific spacer and breakpoint junction sizes.
  • SIT breakpoints were observed at nucleosome midpoints, aligning with Okazaki fragment termini, and SITs were eliminated by DNA polymerase slippage over hairpin structures.

Conclusions:

  • FEN1 plays a significant role in the origination of small inverted triplications (SITs).
  • SIT formation is linked to specific DNA structural features and replication-associated processes.
  • The study provides mechanistic insights into SIT origination and offers tools for studying genome rearrangements.