Microarray hybridization was used to assess acclimation responses to four UV regimes by near isogenic maize (Zea mays) lines varying in flavonoid content. We found that 355 of the 2,500 cDNAs tested were regulated by UV radiation in at least one genotype. Among these, 232 transcripts are assigned putative functions, whereas 123 encode unknown proteins. UV-B increased expression of stress response and ribosomal protein genes, whereas photosynthesis-associated genes were down-regulated; lines lacking UV-absorbing pigments had more dramatic responses than did lines with these pigments, confirming the shielding role of these compounds. Sunlight filtered to remove UV-B or UV-B plus UV-A resulted in significant expression changes in many genes not previously associated with UV responses. Some pathways regulated by UV radiation are shared with defense, salt, and oxidative stresses; however, UV-B radiation can activate additional pathways not shared with other stresses.UV radiation is divided into three classes: UV-C, UV-B, and UV-A. Highly energetic UV-C (wavelengths Յ280 nm) is strongly absorbed by oxygen and ozone in the stratosphere such that none of this sterilizing radiation is present in terrestrial sunlight. Potentially harmful UV-B (280-315 nm) is strongly absorbed by atmospheric ozone, but approximately 4% of terrestrial radiation is UV-B from 290 to 315 nm. UV-A (315-400 nm) is not attenuated by atmospheric ozone, and this less damaging radiation is an important photomorphogenic signal in plant development (Bjorn, 1994). Chlorofluorocarbons and other pollutants have catalyzed depletion of the stratospheric ozone layer; consequently, terrestrial levels of UV-B are increasing with potentially deleterious consequences for all living organisms, particularly for plant development and physiology Searles et al., 2001;Paul and Gwynn-Jones, 2003).UV-B radiation induces diverse morphological and physiological responses in plants (for reviews, see Ballaré et al., 2001;Searles et al., 2001;Paul and Gwynn-Jones, 2003), but the underlying mechanisms governing these integrated responses are unknown. Concurrent with exposure, UV-B photons cause cellular damage by generating photoproducts in DNA (Britt, 1996) and direct damage to proteins (Gerhardt et al., 1999). In response to the inevitable exposure to damaging UV-B radiation, plants have evolved UVinduced mechanisms of protection and repair, such as accumulation of UV-absorbing pigments (Stapleton and Walbot, 1994;Mazza et al., 2000;Bieza and Lois, 2001) and use of UV-A photons to repair most UV-B-induced DNA damage (Britt, 1996). Because of its absorption spectrum, DNA is a major target of UV-B damage; even low doses of radiation can kill mutants lacking specific DNA repair pathways (Britt et al., 1993;Britt, 1996;Landry et al., 1997). In flowering plants, flavonoids, including anthocyanins, accumulate in the vacuoles of epidermal cells where they attenuate the UV component of sunlight with minimal absorption of photosynthetically active radiation (Stapleton and Walbot, 1...