Publication | Open Access
Early signaling components in ultraviolet‐B responses: distinct roles for different reactive oxygen species and nitric oxide
422
Citations
28
References
2001
Year
Nitric OxideLipid PeroxidationMolecular BiologyReactive Oxygen SpeciesRedox BiologyOxidative StressInflammationBiosynthesisReactive Nitrogen SpecieNitric Oxide SynthaseDistinct RolesPhotosynthesisCell SignalingRedox SignalingBiochemistryHeme SignalingReactive Oxygen SpecieGene ExpressionUltraviolet‐b ResponsesCell BiologyBiologySignal TransductionNatural SciencesPhysiologyPhotoprotectionMedicineNitrosative StressPlant PhysiologyLhcb Transcript
The nature and origin of the reactive oxygen species (ROS) involved in the early part of Ultraviolet-B (UV-B)-induced signaling pathways were investigated in Arabidopsis thaliana using a range of enzyme inhibitors and free radical scavengers. The increase in PR-1 transcript and decrease in Lhcb transcript in response to UV-B exposure was shown to be mediated through pathways involving hydrogen peroxide (H(2)O(2)) derived from superoxide (O(2)(&z.rad;-)). In contrast, the up-regulation of PDF1.2 transcript was mediated through a pathway involving O(2)(&z.rad;-) directly. The origins of the ROS were also shown to be distinct and to involve NADPH oxidase and peroxidase(s). The up-regulation of Chs by UV-B was not affected by ROS scavengers, but was reduced by inhibitors of nitric oxide synthase (NOS) or NO scavengers. Together these results suggest that UV-B exposure leads to the generation of ROS, from multiple sources, and NO, through increased NOS activity, giving rise to parallel signaling pathways mediating responses of specific genes to UV-B radiation.
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