In vivo assessment of effect of phytotoxin tenuazonic acid on PSII reaction centers

• TeA inhibited PSII electron transport beyond QA− by occupying the QB site.
• TeA led to a fast conversion of QB reducing centers to non-QB reducing centers.
• TeA decreased sharply the amount of QA or QB reducing centers.
• TeA caused severe inactivation of PSII RCs.
• A model of TeA action is built based on the VJ and PSII RCs.

Tenuazonic acid (TeA), a phytotoxin produced by the fungus Alternaria alternata isolated from diseased croftonweed (Ageratina adenophora), exhibits a strong inhibition in photosystem II (PSII) activity. In vivo chlorophyll fluorescence transients of the host plant croftonweed, show that the dominant effect of TeA is not on the primary photochemical reaction but on the biochemical reaction after QA. The most important action site of TeA is the QB site on the PSII electron-acceptor side, blocking electron transport beyond QA− by occupying the QB site in the D1 protein. However, TeA does not affect the antenna pigments, the energy transfer from antenna pigment molecules to reaction centers (RCs), and the oxygen-evolving complex (OEC) at the donor side of PSII. TeA severely inactivated PSII RCs. The fraction of non-QA reducing centers and non-QB reducing centers show a time- and concentration-dependent linear increase. Conversely, the amount of active QA or QB reducing centers declined sharply in a linear way. The fraction of non-QB reducing centers calculated from data of fluorescence transients is close to the number of PSII RCs with their QB site filled by TeA. An increase of the step-J level (VJ) in the OJIP fluorescence transients attributed to QA− accumulation due to TeA bound to the QB site is a typical characteristic response of the plants leaf with respect to TeA penetration.