Induction of ASCORBATE PEROXIDASE 2 expression in wounded Arabidopsis leaves does not involve known wound-signalling pathways but is associated with changes in photosynthesis

ASCORBATE PEROXIDASE 2 (APX2) encodes a key enzyme of the antioxidant network. In excess light-stressed Arabidopsis leaves, photosynthetic electron transport (PET), hydrogen peroxide (H2O2) and abscisic acid (ABA) regulate APX2 expression. Wounded leaves showed low induction of APX2 expression, and when exposed to excess light, APX2 expression was increased synergistically. Signalling pathways dependent upon jasmonic acid (JA), chitosan and ABA were not involved in the wound-induced expression of APX2, but were shown to require PET and were preceded by a depressed rate of CO2 fixation. This led to an accumulation of H2O2 in veinal tissue. Diphenyl iodonium (DPI), which has been shown previously to be a potent inhibitor of H2O2 accumulation in the veins of wounded leaves, prevented induction of APX2 expression probably by inhibition of PET. Thus, the weak induction of APX2 expression in wounded leaves may require H2O2 and PET only. As in other environmental stresses, wounding of leaves resulted in decreased photosynthesis leading to increased reactive oxygen species (ROS) production. This may signal the induction of many 'wound-responsive' genes not regulated by JA-dependent or other known JA-independent pathways.