Figure 4.

MPK6 mediates UV-B-induced stomatal closure via inducing NO generation in guard cells, and mkp1 hypersensitivity to UV-B-induced NO production and stomatal closure depend on MPK6 activation. A, Leaves of wild-type (WT) Col-0 and Ws, single mutants mpk3-1, mpk3-2, mpk6-1, and mpk6-4, and double mutant mkp1-1/mpk6-1 (mkp1/mpk6) with open stomata were incubated in MES buffer in the absence or presence of 100 µm H₂O₂ or 100 µm SNP under light alone or with 0.5 W m⁻² UV-B for 3 h, then stomatal apertures were measured in epidermal strips from the abaxial surfaces of the treated leaves. Data presented are means ± se of at least three independent experiments, and means with different letters are significantly different at P < 0.01. B to E, Leaves of wild-type Col-0 and Ws and mutants mpk3-1, mpk3-2, mpk6-4, mpk6-1, and mkp1/mpk6 were incubated in MES buffer in the absence or presence of 100 µm H₂O₂ under light alone or with 0.5 W m⁻² UV-B for 3 h, then fluorescence images (B and D) and pixel intensities (C and E) in guard cells preloaded with 50 µm H₂DCFDA (B and C) or 10 µm DAF-2DA (D and E) were recorded. Data of fluorescence intensities are shown as means ± se of three independent experiments, and means with different letters are significantly different at P < 0.05. Bars in B and D = 10 µm.