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Oxidative Stress Induces Telomere Dysfunction and Senescence by Replication Fork Arrest.

Elisa Coluzzi1, Stefano Leone2, Antonella Sgura3

  • 1Department of Science, University of Rome "Roma TRE", Viale Guglielmo Marconi, 446, 00146 Rome, Italy. elisa.coluzzi@uniroma3.it.

Cells
|January 6, 2019
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Oxidative DNA damage, specifically 8-oxoguanine, at telomeres causes replication fork arrest. This leads to telomere dysfunction and cellular senescence, highlighting 8-oxoguanine

Keywords:
epigeneticsoxidative stressreplication forktelomere

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Area of Science:

  • Molecular Biology
  • Genetics
  • Cell Biology

Background:

  • Oxidative DNA damage is frequent in human cells, especially at telomeres.
  • 8-oxoguanine is a major oxidative lesion that can impede DNA replication.
  • Telomere dysfunction is linked to cellular senescence and aging.

Purpose of the Study:

  • To investigate how oxidative damage at telomeres leads to dysfunction and senescence.
  • To elucidate the specific mechanisms of oxidative stress-induced telomere damage.
  • To understand the role of 8-oxoguanine in telomere replication fork stalling.

Main Methods:

  • Induction of acute oxidative stress in human primary fibroblasts.
  • Analysis of telomere-associated proteins (TRF1, TRF2) and DNA damage markers (γH2AX, 53BP1).
  • Chromosome Orientation-FISH (CO-FISH) to assess telomere replication.
  • Analysis of the H3K9me3 histone mark.

Main Results:

  • Oxidative stress reduced TRF1 and TRF2 levels at telomeres.
  • Increased γH2AX relative to 53BP1 indicated replication fork stalls.
  • CO-FISH revealed increased unreplicated telomeres after hydrogen peroxide treatment.
  • H3K9me3 levels increased, suggesting telomere heterochromatinization.

Conclusions:

  • 8-oxoguanine is a key driver of oxidative stress-induced telomere damage.
  • Oxidative damage primarily causes replication fork arrest at telomeres.
  • This replication stress contributes to telomere dysfunction and senescence.