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Abstract
During photosynthesis light energy is converted to chemical energy primarily by thetransfer of electrons through photosysems I and II. However, electrons can also cyclearound photosysems I, generating ATP. Recent studies suggest that along with ATPsynthesis, CET plays a role in photoprotection by mediating nonphotochemicalquenching of excess light and maintaining the proper stromal redox status. There are atleast two partially compensatory CET pathways in most C3 plants, the NAD(P)Hdehydrogenase (NDH)-dependent pathway, and the Proton Gradient Regulation 5(PGR5)-dependent pathway. We analyzed A. thaliana PGR5 (AtPGR5) RNAisuppression lines and over-expressed both the native AtPGR5 and the Pinus taedaPGR5 (PtPGR5) genes in A. thaliana. Compared to wild-type, RNAi plants displayeddecreased NPQ, decreased growth under high light, and increased susceptibility tophotodamage. Constitutive over-expression of AtPGR5 or PtPGR5 caused alterationsin linear and cyclic electron transport, which led to decreased growth under low tomoderate light, but increased tolerance of high light and drought compared to wild-type.AtPGR5:GUS fusions and PtPGR5 tissue-specific northerns indicate that PGR5 ispredominantly expressed in young, rapidly expanding leaves and phloem. Wounding,exposure to excess light and low temperature induce AtPGR5 transcription. Previousresearch indicates that PGR5 expression is suppressed in A. thaliana and P. taedatissues infected biotrophic pathogens. We conclude that PGR5 has an essential,conserved role in protecting plants from excess light energy that may accumulate understress conditions. It is likely that the chloroplast redox status, which is directly affectedby physiological stress, regulates the expression of PGR5. Furthermore, we proposethat NDH-dependent CET cannot compensate for the function of PGR5-dependent CETunder stress conditions.