Thiol regulation of the thylakoid electron transport chain--a missing link in the regulation of photosynthesis?

Abstract

Avoidance of over-reduction of the chloroplast ferredoxin pool is of paramount importance for plants in avoiding oxidative stress. The redox state of this pool can be controlled through regulation of the thylakoid electron transport chain. A model is presented for regulation of this chain via a thiol reduction mechanism, possibly involving a thioredoxin. It is shown in isolated thylakoids that electron transport is inhibited by the thiol reducing agent dithiothreitol. The kinetics of this reduction are rapid and readily reversible. The midpoint redox potential is -365 mV at pH 7.7, with a pH dependency of about -90 mV/pH. At physiological pH values, this places the potential of the species titrated between that of ferredoxin and NADPH and thus in the right potential range to be regulating the redox poise of the ferredoxin pool. This is also close to the potential of NADPH-malate dehydrogenase, an enzyme known to be regulated by thioredoxin. Regulation of electron transport by thioredoxin provides a mechanistic link between the regulation of photosynthesis and gene expression by sugars and the redox regulation of gene expression mediated through the plastoquinone pool.