Abstract
Cyclobutane pyrimidine dimers (CPD) and 6-4 photoproducts are the two prevalent forms of DNA damage caused by UV-B light. By inhibiting DNA replication and transcription, such damage may contribute to the detrimental effects of UV radiation on the growth, productivity, and genetic stability of higher plants. There is however evidence that plants have developed lines of defense against these lesions, such as photoreactivation, nucleotide excision repair, recombination repair, base excision repair and translesion repair. Among these repair systems, photoreactivation is the most effective system where plants cope with UV-induced damage. In addition, plants have mechanisms for tolerating UV damage as a means of avoiding replication fork arrest. Mutant complementation and cDNA analysis have implicated genes isolated from Arabidopsis thaliana in nucleotide excision repair, recombination repair and translesion replication.
