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Related Concept Videos

DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

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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 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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Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...
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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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Translesion (TLS) polymerases rescue stalled DNA polymerases at sites of damaged bases by replacing the replicative polymerase and installing a nucleotide across the damaged site. Doing so, TLS allows additional time for the cell to repair the damage before resuming regular DNA replication.
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Genetic Studies of Human DNA Repair Proteins Using Yeast as a Model System
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Error-free DNA-damage tolerance in Saccharomyces cerevisiae.

Xin Xu1, Susan Blackwell2, Aiyang Lin3

  • 1College of Life Sciences, Capital Normal University, Beijing, 100048, China; Department of Microbiology and Immunology, University of Saskatchewan, Saskatoon, SK, Canada.

Mutation Research. Reviews in Mutation Research
|June 5, 2015
PubMed
Summary

DNA-damage tolerance (DDT) uses sequential PCNA ubiquitination to bypass DNA replication blocks. This review details error-free lesion bypass mechanisms and their interaction with Srs2 and homologous recombination.

Keywords:
DNA-damage toleranceError-free bypassPCNASaccharomyces cerevisiaeSumoylationUbiquitination

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Area of Science:

  • Molecular Biology
  • Genetics
  • Biochemistry

Background:

  • DNA-damage tolerance (DDT) is crucial for cells to overcome replication impediments.
  • In yeast, DDT involves two pathways: error-prone translesion DNA synthesis (TLS) and error-free lesion bypass.
  • Both pathways are regulated by sequential ubiquitination of PCNA at Lys164.

Purpose of the Study:

  • To summarize recent advancements in understanding error-free DDT.
  • To elucidate the molecular mechanisms of error-free lesion bypass.
  • To explore the interplay between error-free DDT, Srs2, and homologous recombination.

Main Methods:

  • Literature review of recent research on DNA-damage tolerance.
  • Analysis of molecular pathways involving PCNA ubiquitination and sumoylation.
  • Integration of findings on TLS, error-free bypass, Srs2, and homologous recombination.

Main Results:

  • PCNA monoubiquitination by Rad6-Rad18 activates TLS.
  • Lys63-linked polyubiquitination of PCNA by Mms2-Ubc13-Rad5 promotes error-free bypass.
  • PCNA sumoylation recruits Srs2, a helicase and anti-recombinase.

Conclusions:

  • The molecular details of error-free lesion bypass remain incompletely understood.
  • Error-free DDT pathways are intricately linked with Srs2 and homologous recombination.
  • Further research is needed to fully characterize these complex DNA repair mechanisms.