Mechanisms of Eukaryotic DNA Double Strand Break Repair

Front Biosci. 2006 May 1;11:1958-76. doi: 10.2741/1938.

Abstract

For all cells, a DNA double strand break (DSB) is a dangerous lesion that can have profound consequences for the genome. If a DSB is encountered during mitosis, chromosomal separation may be adversely affected. Alternatively, during S phase a DSB may cause replication fork stalling or collapse. Improperly repaired DSBs can result in chromosomal rearrangements, senescence or activation of apoptotic pathways. Cells have developed sophisticated recombination pathways to metabolize and repair DSBs quickly as well as the capacity to differentiate physiologically occurring breaks from life threatening lesions. The two major pathways of recombination repair are known as non-homologous end-joining (NHEJ) and homologous recombination (HR). In this review, we will discuss the detection, response, and repair of DSBs in eukaryotes.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Antigens, Nuclear / metabolism
  • Apoptosis
  • Cell Differentiation
  • Cellular Senescence
  • Chromosome Pairing
  • DNA Damage*
  • DNA Helicases / chemistry
  • DNA Repair*
  • DNA-Activated Protein Kinase / chemistry
  • DNA-Binding Proteins / metabolism
  • Models, Genetic
  • Recombination, Genetic
  • S Phase
  • Saccharomyces cerevisiae / metabolism
  • Saccharomyces cerevisiae Proteins / metabolism

Substances

  • Antigens, Nuclear
  • DNA-Binding Proteins
  • Saccharomyces cerevisiae Proteins
  • DNA-Activated Protein Kinase
  • DNA Helicases