Blocking the QB‐binding site of photosystem II by tenuazonic acid, a non–host‐specific toxin of Alternaria alternata, activates singlet oxygen‐mediated and EXECUTER‐dependent signalling in Arabidopsis

Abstract Necrotrophic fungal pathogens produce toxic compounds that induce cell death in infected plants. Often, the primary targets of these toxins and the way a plant responds to them are not known. In the present work, the effect of tenuazonic acid ( TeA ), a non–host‐specific toxin of A lternaria alternata , on A rabidopsis thaliana has been analysed. TeA blocks the Q B ‐binding site at the acceptor side of photosystem II ( PSII ). As a result, charge recombination at the reaction centre ( RC ) of PSII is expected to enhance the formation of the excited triplet state of the RC chlorophyll that promotes generation of singlet oxygen ( 1 O 2 ). 1 O 2 activates a signalling pathway that depends on the two EXECUTER ( EX ) proteins EX 1 and EX 2 and triggers a programmed cell death response. In seedlings treated with TeA at half‐inhibition concentration 1 O 2 ‐mediated and EX ‐dependent signalling is activated as indicated by the rapid and transient up‐regulation of 1 O 2 ‐responsive genes in wild type, and its suppression in ex 1/ ex 2 mutants. Lesion formation occurs when seedlings are exposed to higher concentrations of TeA for a longer period of time. Under these conditions, the programmed cell death response triggered by 1 O 2 ‐mediated and EX ‐dependent signalling is superimposed by other events that also contribute to lesion formation.