摘要
Light is emerging as a central regulator of plant immune responses against herbivores and pathogens. Solar UVoB radiation plays an important role as a positive modulator of plant defense. However, since UV-B photons can interact with a wide spectrum of molecular targets in plant tissues, the mechanisms that mediate their effects on plant defense have remained elusive. Here, we show that ecologically meaningful doses of UV-B radiation increase Arabidopsis resis- tance to the necrotrophic fungus Botrytis cinerea and that this effect is mediated by the photoreceptor UVR8. The UV-B effect on plant resistance was conserved in mutants impaired in jasmonate （JA） signaling （jar1-1 and P35S：JAZlO.4） or metabolism of tryptophan-derived defense compounds （pen2-1, pacl3-1, pen2 pad3）, suggesting that neither regulation of the JA pathway nor changes in levels of indolic glucosinolates （iGS） or camalexin are involved in this response. UV-B radiation, acting through UVR8, increased the levels of flavonoids and sinapates in leaf tissue. The UV-B effect on pathogen resistance was still detectable in tt4-1, a mutant deficient in chalcone synthase and therefore impaired in the synthesis of flavonoids, but was absent in fahl-7, a mutant deficient in ferulic acid 5-hydroxylase, which is essential for sinapate bio- synthesis. Collectively, these results indicate that UVR8 plays an important role in mediating the effects of UV-B radiation on pathogen resistance by controlling the expression of the sinapate biosynthetic pathway.
Light is emerging as a central regulator of plant immune responses against herbivores and pathogens. Solar UVoB radiation plays an important role as a positive modulator of plant defense. However, since UV-B photons can interact with a wide spectrum of molecular targets in plant tissues, the mechanisms that mediate their effects on plant defense have remained elusive. Here, we show that ecologically meaningful doses of UV-B radiation increase Arabidopsis resis- tance to the necrotrophic fungus Botrytis cinerea and that this effect is mediated by the photoreceptor UVR8. The UV-B effect on plant resistance was conserved in mutants impaired in jasmonate （JA） signaling （jar1-1 and P35S：JAZlO.4） or metabolism of tryptophan-derived defense compounds （pen2-1, pacl3-1, pen2 pad3）, suggesting that neither regulation of the JA pathway nor changes in levels of indolic glucosinolates （iGS） or camalexin are involved in this response. UV-B radiation, acting through UVR8, increased the levels of flavonoids and sinapates in leaf tissue. The UV-B effect on pathogen resistance was still detectable in tt4-1, a mutant deficient in chalcone synthase and therefore impaired in the synthesis of flavonoids, but was absent in fahl-7, a mutant deficient in ferulic acid 5-hydroxylase, which is essential for sinapate bio- synthesis. Collectively, these results indicate that UVR8 plays an important role in mediating the effects of UV-B radiation on pathogen resistance by controlling the expression of the sinapate biosynthetic pathway.
