M Z Zdzienicka1. 1. MGC-Department of Radiation Genetics and Chemical Mutagenesis, Leiden University, The Netherlands. Zdzienicka@rullf2.MedFac.LeidenUniv.nl
Abstract
BACKGROUND: DNA double-strand breaks (DSB) are the most genotoxic lesions induced by ionizing radiation. At least 2 different pathways for DSB repair have been identified, homologous and non-homologous recombination. METHODS: Studies on X-ray-sensitive mutants have led to the identification of several genes involved in processing of DSB in bacteria, yeast and mammalian cells. RESULTS AND CONCLUSION: In mammalian cells non-homologous recombination is the main pathway for DSB repair, while the role of homologous recombination in DSB repair awaits clarification. It is known that, in addition to DNA repair, other safeguards control the human cellular response to ionizing radiation, such as cell cycle regulation and mechanisms involved in scavenging of free radicals produced by ionizing radiation.
BACKGROUND: DNA double-strand breaks (DSB) are the most genotoxic lesions induced by ionizing radiation. At least 2 different pathways for DSB repair have been identified, homologous and non-homologous recombination. METHODS: Studies on X-ray-sensitive mutants have led to the identification of several genes involved in processing of DSB in bacteria, yeast and mammalian cells. RESULTS AND CONCLUSION: In mammalian cells non-homologous recombination is the main pathway for DSB repair, while the role of homologous recombination in DSB repair awaits clarification. It is known that, in addition to DNA repair, other safeguards control the human cellular response to ionizing radiation, such as cell cycle regulation and mechanisms involved in scavenging of free radicals produced by ionizing radiation.
Authors: K O Hartley; D Gell; G C Smith; H Zhang; N Divecha; M A Connelly; A Admon; S P Lees-Miller; C W Anderson; S P Jackson Journal: Cell Date: 1995-09-08 Impact factor: 41.582