DYNAMICS OF PHOTOSYSTEM-II HETEROGENEITY DURING PHOTOINHIBITION - DEPLETION OF PS-II-BETA FROM NON-APPRESSED THYLAKOIDS DURING STRONG-IRRADIANCE EXPOSURE OF CHLAMYDOMONAS-REINHARDTII

Thylakoid membranes of Chlamydomonas reinhardtii were fractionated into appressed membranes and non-appressed vesicles. The latter had a Chl a/b ratio of 3.2 and contained 1.12 mmol PS II (mol Chl a + b)-1. The PS II centers in the non-appressed regions displayed the kinetic characteristics of PS II-beta centers. They were able to generate a stable charge-separation to Q(A), but they were unable to transfer electrons from Q(A-) to Q(B) (Q(B)-nonreducing centers). After a strong-irradiance treatment (SIT) of cells by exposure to 2000-mu-mol . m-2 . s-1 for 15 min, a portion of the PS II-alpha centers in the appressed membranes was damaged due to photoinhibition. PS II-beta centers were resistant to photoinhibitory damage; however, SIT caused a lowering of the PS II content in the non-appressed fraction to 0.60 mmol PS II (mol Chl a + b)-1. Concomitantly, there was a conversion of Q(B)-nonreducing centers to a form able to reduce the plastoquinone pool (Q(B)-reducing centers). Low-temperature during SIT inhibited both the depletion of PS II-beta from the non-appressed membrane region and the activation of Q(B)-nonreducing centers. These results are consistent with a 'PS II repair cycle' which translocates PS II units from the stroma-exposed membranes into the appressed thylakoids during activation of PS II-beta from a Q(B)-nonreducing to a Q(B)-reducing form. Since the overall distribution of Chl-protein complexes between the stroma-exposed and appressed membrane regions was unaffected by SIT, it is suggested that damaged PS II units from the appressed membrane region are exchanged with PS II-beta from the stroma-exposed membranes.