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Journal article

Tissue specificity in DNA repair: lessons from trinucleotide repeat instability.

  • Dion V University of Lausanne, Center for Integrative Genomics, Bâtiment Génopode, 1015 Lausanne, Switzerland. Electronic address: vincent.dion@unil.ch.
  • 2014-05-21
Published in:
  • Trends in genetics : TIG. - 2014
DNA repair
base excision repair
genome stability
nucleotide excision repair
single-strand break repair
tissue-specific DNA repair
trinucleotide repeat instability
Animals
DNA Damage
DNA Repair
Genomic Instability
Humans
Organ Specificity
Trinucleotide Repeats
English DNA must constantly be repaired to maintain genome stability. Although it is clear that DNA repair reactions depend on cell type and developmental stage, we know surprisingly little about the mechanisms that underlie this tissue specificity. This is due, in part, to the lack of adequate study systems. This review discusses recent progress toward understanding the mechanism leading to varying rates of instability at expanded trinucleotide repeats (TNRs) in different tissues. Although they are not DNA lesions, TNRs are hotspots for genome instability because normal DNA repair activities cause changes in repeat length. The rates of expansions and contractions are readily detectable and depend on cell identity, making TNR instability a particularly convenient model system. A better understanding of this type of genome instability will provide a foundation for studying tissue-specific DNA repair more generally, which has implications in cancer and other diseases caused by mutations in the caretakers of the genome.
Language
  • English
Open access status
green
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Persistent URL
https://sonar.ch/global/documents/20258
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