• P C Hanawalt.
• Department of Biological Sciences, Stanford University, CA 94305-5020.
• Environ. Mol. Mutagen. 1989 Jan 1; 14 Suppl 16: 90-8.

AbstractMuch of our early understanding of the mechanisms of excision-repair and its roles in maintaining genome integrity and cellular viability was derived from studies with bacteria. In fact, the discoveries of damage excision and repair replication were made in ultraviolet (UV)-irradiated Escherichia coli. Recent advances in recombinant DNA technology have helped to further our understanding of the manner in which mammalian cells deal with damage in their complex genomes. These include the discovery that expressed genes may be preferentially repaired and, furthermore, that the transcribed DNA strand, for some types of damage, is selectively repaired within an active gene. The latter finding has now been documented in E. coli as well, so it is likely that it is of widespread importance as a mechanism to ensure the expression of active genes in otherwise damaged cells. It is certain that studies with bacterial systems as models will continue to have an important impact on the development of the field of mammalian DNA repair.

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