DNA double-strand breaks repair pathways in the framework of chromatin

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DNA double-strand breaks are defined are two simultaneous nicks in opposite strands of the DNA helix, which are in sufficiently close proximity to one another that base-pairing and chromatin structure are unable to maintain the broken DNA ends juxtaposed. These lesions arise in the course of normal and pathological endogenous DNA metabolism or can result from exogenous agents such as ionizing radiation and certain chemotherapeutic drugs. They represent the most severe type of DNA damage with respect to preservation of genomic integrity and there is growing evidence suggesting that in higher eukaryotes aberrant repair of double-strand breaks is a key event in carcinogenesis. Therefore, cells have evolved complex mechanisms that include cell cycle arrest, activation and increased expression of various genes including those associated with DNA repair and in certain cases induction of the apoptotic pathway, to respond to double-strand breaks. Given the intense research effort in this field in the past few years our knowledge of the molecular details relating to the detection, signalling and repair of double-strand breaks has greatly increased. Here we discuss recent progress in our understanding of molecular responses to DNA double-strand breaks with a particular emphasis on homologous recombination and non-homologous end-joining, the major double-strand break repair pathways. In addition, the role of changes in chromatin architecture in response to double-strand breaks is currently emerging and already numerous links between changes in chromatin-resulting from both the contribution of histone tail modifications and chromatin remodelling complexes-and repair pathways have been made. Therefore, the importance of epigenetic modifications in the doublestrand break repair pathways will also be discussed.

Original languageEnglish
Title of host publicationNew Research on DNA Repair
PublisherNova Science Publishers
Number of pages30
ISBN (Print)9781600213854
Publication statusPublished - 1 Dec 2007
Externally publishedYes


  • Chromatin remodelling
  • Double-strand breaks
  • Histone modifications
  • Homologous recombination
  • Nonhomologous end-joining
  • Signal transduction

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