The role of different photoprotection mechanisms in preventing photoinhibition of Photosystem

Light is fundamental for photosynthesis. However, when in excess, it may produce reactive oxygen species (ROS) which, in turn, may damage the Photosystem II reaction center D1 protein. In order to avoid this, photosynthetic organisms have developed different mechanisms able to protect their photosynthetic apparatus. The term photoprotection is used to define all these process. Higher plants have evolved different protective mechanisms which are: the thermal dissipation through NPQ depending on PSBS protein, phosphorylation of LHCII to ensure efficient distribution of light energy between photosystems (state transition) depending on STNZ/TAP38 kinase/phosphatase system and Cyclic Electron Flow/ Photosynthetic Control (CEF/PC) around PSI depending on PGR5/PGRL1A/B proteins. However, how this mechanisms affect D1 turnover is not know. Much of current knowledge about photoprotection comes from studies with knock Arabidopsis thaliana in which respective key genes have been inactivated. In this work, this genetic approach was extended by generating, by crossing, high order mutants where two (ASL, 455) or all three (48L78) photoprotection mechanisms have been eliminated. These mutants have been characterized and their light sensibility investigated, by using fluorescence (PSII), absorbance changes (PSI), protein phosphorylation and turnover of D1 protein by immunoblotting. Although all the mechanisms seems to be important in plants photoprotection, the sensibility of PSII to light is more marked in mutants where CEF/PC is absent and this is paralleled by an increase in D1 turnover. PSI is also highly damaged by light, but, if lincomycin is present, it resulted protected. In AS mutant the sensibility to light, in terms of PSII efficiency, is not as marked as it could be expected but the D1 turnover is very high.