Passive Entry of CO₂ and Its Energy-dependent Intracellular Conversion to HCO₃^- in Cyanobacteria Are Driven by a Photosystem I-generated ΔμH⁺

CO₂ entry into Synechococcus sp. PCC7942 cells was drastically inhibited by the water channel blocker p-chloromercuriphenylsulfonic acid suggesting that CO₂ uptake is, for the most part, passive via aquaporins with subsequent energy-dependent conversion to HCO₃ ^-. Dependence of CO₂ uptake on photosynthetic electron transport via photosystem I (PSI) was confirmed by experiments with electron transport inhibitors, electron donors and acceptors, and a mutant lacking PSI activity. CO₂ uptake was drastically inhibited by the uncouplers carbonyl cyanide m-chlorophenylhydrazone (CCCP) and ammonia but substantially less so by the inhibitors of ATP formation arsenate and N,N,-dicyclohexylcarbodiimide (DCCD). Thus a ΔμH⁺ generated by photosynthetic PSI electron transport apparently serves as the direct source of energy for CO₂ uptake. Under low light intensity, the rate of CO₂ uptake by a high-CO₂-requiring mutant of Synechococcus sp. PCC7942, at a CO₂ concentration below its threshold for CO₂ fixation, was higher than that of the wild type. At saturating light intensity, net CO₂ uptake was similar in the wild type and in the mutant IL-3 suggesting common limitation by the rate of conversion of CO₂ to HCO₃^-. These findings are consistent with a model postulating that electron transport-dependent formation of alkaline domains on the thylakoid membrane energizes intracellular conversion of CO₂ to HCO₃^-.