UV-B radiation damages a variety of cellular components. A plant's ability to resist the effects of UV is a product of its ability to reduce exposure (through the optimization of growth pattern and the production of UV absorbing pigments) and its ability to repair or replace damaged molecules. The expression of these UV resistance mechanisms is sensitive to the quantity and quality of ambient light. In the present study the significance of DNA repair as a UV resistance mechanism in Arabidopsis was investigated by comparing the effects of solar UV on the growth of a variety of repair-proficient and -deficient Arabidopsis lines grown under natural light, focusing on the effects of UV on the growth of well-established plants. It was found that solar UV had an inhibitory effect on the growth of wild-type plants, and that this effect is enhanced in repair-defective lines. Plants defective in the cyclobutane dimer photolyase are most sensitive to the effects of UV-B on plant height and rosette diameter growth, indicating that, at least in this Arabidopsis ecotype and at this stage of growth, this enzyme plays an important role in UV resistance. A mutant defective in nucleotide excision repair (NER), a non-specific repair pathway, also displayed a significant, though lesser, sensitivity to solar UV-B, suggesting that either the transcription-coupled repair of UV-induced dimers, or the repair of some other UV-induced lesion, is also important for optimal growth. The relatively mild enhancement of UV sensitivity in repair-defective Arabidopsis stands in dramatic contrast to the immediate, severe, and ultimately lethal effects of sunlight on repair-defective (XP) humans.