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The pho1 mutant of Arabidopsis has been shown to respond to the phosphate deficiency in the leaves by decreasing the amount of phosphatidylglycerol (PG). PG is thought to be of crucial importance for the organization and function of the thylakoid membrane. This prompted us to ask what the consequences of the PG deficiency may be in the pho1 mutant when grown under low or high light. While in the wild-type, the lipid pattern was almost insensitive to changes in the growth light, PG was reduced to 45% under low light in the mutant, and it decreased further to 35% under high light. Concomitantly, sulfoquinovosyl diacylglycerol (SQDG) and to a lesser extent digalactosyl diacylglycerol (DGDG) increased. The SQDG increase correlated with increased amounts of the SQD1 protein, an indicator for an actively mediated process. Despite of alterations in the ultrastructure, mutant thylakoids showed virtually no effects on photosynthetic electron transfer, O2 evolution and excitation energy allocation to the reaction centers. Our results support the idea that PG deficiency can at least partially be compensated for by the anionic lipid SQDG and the not charged lipid DGDG. This seems to be an important strategy to maintain an optimal thylakoid lipid milieu for vital processes, such as photosynthesis, under a restricted phosphate availability.

The lipid content of a Photosystem II preparation, derived by Triton X-100 fractionation of spinach thylakoid membranes, which retained high rates of oxygen evolution was examined. It was found that the detergent treatment resulted in a preferential loss of digalactosyldiacylglycerol. The effect on this preparation of exogenously added lipids, or lipid mixtures, purified from thylakoids was investigated. Addition of total polar lipid extract stimulated the rates of oxygen evolution, the same effect being achieved with isolated digalactosyldiacylglycerol or phosphatidylcholine alone. The stimulation of oxygen evolution was dependent on the degree of unsaturation of the lipids used and on the relative amounts of acidic lipids present in the mixtures. Addition of isolated acidic lipids alone resulted in a complete inhibition of oxygen evolution. The results are discussed in terms of the possible involvement of thylakoid lipids in the molecular organisation of the Photosystem II oxygen-evolving system.

The recovery of O2 evolution of cholate-treated thylakoids induced by the simultaneous addition of the 17- and 23-kDa proteins was enhanced by the further addition of thylakoid total lipids up to about 75% of the non-depleted original broken thylakoids at the optimal concentration of the lipids, through reactivation of electron transfer between the sites of DPC donation and DCIP acceptance. Novel findings clarifing the cause of the discrepancies, with regard to the requirement for the 17-kDa protein on the O2 evolution of thylakoid membranes, were also provided, i.e., when the assay of O2 evolution for the reconstituted systems was carried out at a low level of NaCl (e.g., 0.1 mM), besides the 23-kDa protein, the 17-kDa protein was also required for O2 evolution, however, at a higher level of NaCI (>5 mM) the 17-kDa protein was not. The results suggest that the 17-kDa protein takes the place of Cl− or acts as a constituent protecting C− in the Cl− activating sites against fluctuation of the Cl− level in the inner compartment of thylakoid membranes.