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In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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In order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
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APOBEC3A damages the cellular genome during DNA replication.

Abby M Green1,2, Sébastien Landry3, Konstantin Budagyan4

  • 1a Division of Oncology , Department of Pediatrics , Children's Hospital of Philadelphia and University of Pennsylvania Perelman School of Medicine , Philadelphia , PA , USA.

Cell Cycle (Georgetown, Tex.)
|February 27, 2016
PubMed
Summary

The DNA-cytosine deaminase APOBEC3A (A3A) damages replicating cells by targeting single-stranded DNA at replication forks. This leads to cell cycle arrest and DNA breaks, contributing to genome instability in tumors.

Keywords:
APOBEC3ATR kinaseDNA replicationDNA replication stresscell cycle checkpointcytosine deaminationsingle-stranded DNA

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Area of Science:

  • Genetics
  • Molecular Biology
  • Cancer Research

Background:

  • The human APOBEC3 (A3) family comprises DNA-cytosine deaminases that restrict viral infections by mutating viral DNA.
  • Evidence suggests A3 enzymes can damage the host genome, with mutational signatures found in tumor DNA.
  • Mechanisms producing single-stranded DNA (ssDNA) substrates for A3 deamination in mammalian cells remain unclear.

Purpose of the Study:

  • To investigate single-stranded DNA (ssDNA) at replication forks as a substrate for APOBEC3 deamination.
  • To elucidate the mechanisms of A3-induced DNA damage in cellular genomes.

Main Methods:

  • Studied APOBEC3A (A3A) expression in replicating versus quiescent cells.
  • Assessed DNA damage, cell cycle progression, and replication checkpoint activation.
  • Investigated cellular vulnerability to A3A-induced damage under replication stress.

Main Results:

  • A3A expression causes DNA damage in replicating cells, but not quiescent cells.
  • Cycling cells expressing A3A activate the DNA replication checkpoint and arrest.
  • Replication stress increases cellular vulnerability to A3A-induced DNA damage.

Conclusions:

  • A model is proposed where A3A deaminates cytosines at replication forks and other ssDNA substrates, causing mutations and DNA breaks.
  • A3A expression poses a mutagenesis risk in replicating progenitor cells.
  • APOBEC3 enzymes likely contribute to genome instability observed in human tumors.