Ultraviolet B radiation enhances a phytochrome-B-mediated photomorphogenicresponse in Arabidopsis

Ultraviolet B radiation (UV-B, 290-315 nm) can cause damage and induce phot omorphogenic responses in plants. The mechanisms that mediate the photomorp hogenic effects of UV-B are unclear. In etiolated Arabidopsis seedlings, a daily exposure to 2.5 h of UV-B enhanced the cotyledon opening response ind uced by a subsequent red light (R) pulse. An R pulse alone, 2.5 h of UV-B t erminated with a far-red pulse, or 2.5 h of continuous R caused very little cotyledon opening. The enhancing effect of UV-B increased with fluence rat e up to approximately 7.58 mu mol m(-2) s(-1) at higher fluence rates the r esponse to UV-B was greatly reduced. The phyA, phyA cry1, and cry1 cry2 mut ants behaved like the wild type when exposed to UV-B followed by an R pulse . Ln contrast, phyB, phyB cry1, and phyB phyA mutants failed to spell the c otyledons. Thus, phytochrome B was required for the cotyledon opening respo nse to UV-B --> R treatments, whereas phytochrome A and cryptochromes 1 and 2 were not necessary under the conditions of our experiments. The enhancin g effect of lo-ti doses of UV-B on cotyledon opening in uvr1 uvr2 and uvr1 uvr3 mutants, deficient in DNA repair, was similar to that found in the wil d type, suggesting that this effect of UV-B was not elicited by signals der ived from UV-B-induced DNA lesions (cyclobutane pyrimidine dimers and 6-4 p hotoproducts). We conclude that low doses of UV-B, perceived by a receptor system different from phytochromes, cryptochromes, or DNA, enhance a de-eti olation response that is induced by active phytochrome B.