Abstract
The requirement of HCO3− (or CO2) for stimulating the electron flow at the acceptor side of photosystem II (which is a different role from that in CO2 fixation) in spinach leaf discs and in Chlamydomonas cells, both pretreated with formate, is presented. Short formate-treatment produces a quenching of the maximum chlorophyll a fluorescence and decreases the rate of O2 evolution; addition of HCO3− reverses both inhibitions. The same fluorescence quenching is observed in the presence of hydroxylamine as an electron donor suggesting that this site of anion action is between the electron donor “Z” and the primary plastoquinone QA. Long formate-treatment slows down the decay of variable fluorescence which is similar to that caused by DCMU-treatment; HCO3− addition accelerates this decay suggesting that this site of anion action is between QA and the plastoquinone (PQ) pool. Furthermore, addition of HCO3− to HCO2− treated samples produces 4 fold stimulation of the Hill reaction in the presence of DEMIB that inhibits electron flow between the two photosystems and, thus, CO2 fixation. We suggest that, in spinach leaves and Chlamydomonas, HCO3− regulates the reactions of PS II from Z (or D) to QA and from QA to the PQ pool.