PARENT SESSION

Symposium S2B Light, redox and metabolic regulation: Light reactions
Monday August 30th, 2004 2:40 PM-4:40 PM Room 210A
Chair: Frances-Andre Wollman
Co-Chair: Kris Niyogi

Modulation of CFO-CF1 ATP synthase conductivity and proton motive force (pmf) partitioning regulate light capture. Tom Avenson^*,1, Jeffrey Cruz¹, David Kramer¹, ¹ Washington State University, Pullman, WA, USA

ABSTRACT- Photosynthetic energy conversion is regulated at multiple levels to prevent photodamage to the photosynthetic apparatus at various sites. Light capture is regulated by energy dependent quenching of excitons (qE), the predominant component of non-photochemical quenching of excitation energy, which functions to harmlessly dissipate excessively absorbed light energy as heat prior to it entering the energy storing redox reactions of photosystem II (PSII). qE is activated by conversion of violaxanthin to zeaxanthin and protonation of lumen-exposed residues of psbS, an intrinsic polypeptide of the light harvesting complex of PSII, both mechanisms of which are dependent upon lumen acidification. Since qE is pH dependent, and because various mechanisms can alter the pH of the lumen, there are multiple models to account for qE modulation, a necessary feature of light energy conversion that is due, in part, to fluctuating biochemical demands. Although lumen acidification will obviously be a function of light driven electron transfer and its associated proton pumping, it has become clear that modulation of proton efflux from the lumen, primarily controlled by the conductivity of the ATP synthase, and differential partitioning of the proton motive force (pmf), e.g. storing more/less of the pmf as a pH gradient, are mechanisms that can also alter the pH of the lumen at a given flux of protons. We present in vivo evidence that lowering [CO2] and [O2] to 50 ppm and 1%, respectively, resulted in increased sensitization of qE to linear electron flow, an effect that was partially attributable to changes in ATP synthase conductivity, but was also found to be due to increased storage of pmf as a pH gradient. We discuss these findings in the context of the need for mechanisms that modulate qE without altering the ATP/NADPH output ratio, as occurs with mechanisms that increase proton translocation into the lumen (i.e. cyclic electron flow around photosystem I).

KEY WORDS: ATP synthase conductivity, proton motive force partitioning, qE modulation