Antimycin A induces light hypersensitivity of photosystem II in the presence of QB-site binding herbicides

Abstract

AbstractPhotosynthetic electron transport consists of linear electron flow and two cyclic electron flow (CEF) pathways around photosystem I (PSI). PGR5-dependent CEF-PSI is thought to be the major CEF-PSI pathway and an important regulator of photosynthetic electron transfer. Antimycin A (AA) is commonly recognized as an inhibitor of PGR5-dependent CEF-PSI in photosynthesis. Although previous findings imply that AA may also affect photosystem II (PSII), which does not participate in CEF-PSI, these “secondary effects” tend to be neglected, and AA is often used for inhibition of PGR5-dependent CEF-PSI as if it were a specific inhibitor. Here, we investigated the direct effects of AA on PSII using isolated spinach PSII membranes, and spinach andChlamydomonasthylakoid membranes. Measurements of QA−reoxidation kinetics showed that AA affects the acceptor side of PSII and inhibits electron transport within PSII. Furthermore, repetitiveFv/Fmmeasurements revealed that, in the presence of QB-site binding inhibitors, AA treatment results in severe photoinhibition even from a single-turnover flash. The direct effects of AA on PSII are non-negligible and caution is required when using AA as an inhibitor of PGR5-dependent CEF-PSI. Meanwhile, we found that the commercially available compound AA3, which is a component of the AA complex, inhibits PGR5-dependent CEF-PSI without having notable effects on PSII. Thus, we propose that AA3 should be used for the physiological study of the PGR5-dependent CEF-PSI.