Radiation inducible DNA repair processes in eukaryotes

Eukaryotic cells respond to radiation-induced damage in DNA and other cellu lar components by turning on cascades of regulatory events which constitute a complex network of pathways of cell cycle checkpoints, DNA repair and da mage tolerance mechanisms, recombination and delayed cell death (apoptosis) . By virtue of the high homology in structure and function of yeast and mam malian proteins several DNA repair pathways that may be upregulated in resp onse to radiation, and some of their regulatory factors involved in sensing of damage, signal transduction by protein kinase cascades and transcriptio n have been identified. In yeast, genes for DNA synthesis and replicative d amage bypass, for base and nucleotide excision repair, in particular global genome repair, and for crucial steps in DNA double strand break repair by homologous recombination show enhanced expression in response to radiation. In mammalian cells, the identification of homologous genes and upregulated homologous DNA repair pathways makes fast progress. It is, however, eviden t that the regulatory network is considerably more complex than in yeast. T he improved understanding on the molecular level of the radiation-inducible cellular responses to radiation is of high public interest. Especially, th e response to very low doses may have relevance for the risk estimation for ionising radiation and, possibly as well, ultraviolet light (UV-B), and fo r the design of suitable dose fractionation schemes for radiotherapy. (C) S ociete francaise de biochimie et biologie moleculaire / Elsevier, Paris.