Depletion of stromal P(i) induces high 'energy-dependent' antenna exciton quenching (q(E)) by decreasing proton conductivity at CF(O)-CF(1) ATP synthase.

This work tests two models to account for the effects of depletion of stromal inorganic phosphate (P(i)), which results in down-regulation of light capture via the exciton quenching (q(E)) mechanism and has been proposed to act in feedback regulation of the light reactions. In both models, antenna down-regulation is activated by acidification of the lumen, despite the fact that linear electron flow (LEF) (and associated proton flux) is decreased upon P(i) depletion. In one model, an imbalance of ATP or NADPH activates cyclic electron transfer around photosystem I (CEF1), increasing proton influx to the lumen. In the second, the effective conductivity of the CF(O)-CF(1) ATP synthase to protons (g(H)(+)) is decreased, retarding proton efflux from the lumen. Sequestering of P(i) by mannose infiltration increased sensitivities of q(E) and pmf to LEF. The effects were attributable to decreases in g(H)(+), but not to CEF1 and were largely reversed by subsequent P(i) feeding. Rapid recovery of g(H)(+) in the dark suggested that dark-labile metabolic pools are responsible for regulation of the ATP synthase. Overall, these results support models where accumulation of Benson-Calvin cycle intermediates or lowering of stromal P(i) below its K(M)at the ATP synthase, retards proton efflux from the lumen, leading to build-up of pmf and subsequent down-regulation of photosynthetic light capture.