Huner NPA, Ivanov AG, Sane PV, Pocock T, Król M, Balseris A, Rosso D, Savitch LV, Hurry VM, Öquist G
Photoprotection of Photosystem II: Reaction center quenching versus antenna quenching
In: Photoprotection, Photoinhibition, GeneRegulation and Environment, Springer 2005, pp. 155-174

Understanding the role of the xanthophyll cycle and elucidating the mechanisms of antenna quenching through the non-photochemical dissipation of excess absorbed energy in the photoprotection of the photochemical apparatus continues to be a major focus of photosynthetic research. In addition to antenna quenching, there is evidence for the non-photochemical dissipation of excess energy through the PS II reaction center. Hence, this photoprotective mechanism is called reaction center quenching. One technique to assess reaction center quenching is photosynthetic thermoluminescence. This technique represents a simple but powerful probe of PS II photochemistry that measures the light emitted due to the reversal of PS II charge separation through the thermally-dependent recombination of the negative charges stabilized on QA- and QB- on the acceptor side of PS II with the positive charges accumulated in the S2- and S3-states of the oxygen evolving complex. Changes in the temperature maxima for photosynthetic thermoluminescence reflect changes in redox potentials of recombining species within PS II reaction centers. Exposure of Synechococcus sp. PCC 7942, Pinus sylvestris L., Arabidopsis thaliana, and Chlamydomonas reinhardtii to either low temperatures or to high light induces a significant downshift in the themperature maxima for S2QB- and S3QB- recombinations relative to S2QA- and S3QA- recombinations. These shifts in recombination temperatures are indicative of lower activation energy for the S2QB- redox pair recombination and a narrowing of the free energy gap between QA and QB electron acceptors. This, in turn, is associated with a decrease in the overall thermoluminescence emission. We propose that environmental factors such as high light and low temperature result in an increased population of reduced QA (QA-), that is, increased excitation pressure, facilitating non-radiative P680+QA- radical pair recombination within the PS II reaction center. The underlying molecular mechanisms regulating reaction center quenching appear to be species dependent. We conclude that reaction center quenching and antenna quenching are complementary mechanisms that may function to protoprotect PS II to different extents in vivo depending on the species as well as the environmental conditions to which the organism is exposed.