Abstract
An ultraviolet-B (UV-B)-resistant mutant, uvi1 (UV-B insensitive 1), of Arabidopsis was isolated from 1,280 M(1) seeds that had been exposed to ion beam irradiation. The fresh weight of uvi1 under high-UV-B exposure was more than twice that of the wild type. A root-bending assay indicated that root growth was less inhibited by UV-B exposure in uvi1 than in the wild type. When the seedlings were grown under white light, the UV-B dose required for 50% inhibition was about 6 kJ m(-2) for the wild type and 9 kJ m(-2) for uvi1. When the seedlings were irradiated with UV-B in darkness, the dose required for 50% inhibition was about 1.5 kJ m(-2) for the wild type and 4 kJ m(-2) for uvi1. An enzyme-linked immunosorbent assay showed that the reduction in levels of cyclobutane pyrimidine dimers (CPDs) under white light and of (6-4) photoproducts in darkness occurred faster in uvi1 than in the wild type. These results indicate that uvi1 had increased photoreactivation of CPDs and dark repair of (6-4) photoproducts, leading to strong UV-B resistance. Furthermore, the transcript levels of PHR1 (CPD photolyase gene) were much higher in uvi1 than in the wild type both under white light and after UV-B exposure. Placing the plants in the dark before UV-B exposure decreases the early reduction of CPDs in the wild type but not in uvi1. Our results suggest that UVI1 is a negative regulator of two independent DNA repair systems.