Two distinct redox signaling pathways for cytosolic APX induction under photooxidative stress.

The cross-talk of two redox factors, H2O2 accumulation and redox status of photosynthetic electron transport (PET) in tobacco chloroplasts, on the expression of cytosolic ascorbate peroxidase (cAPX) was studied. Transgenic tobacco plants, which expressed respectively the Escherichia coli catalase and spinach thylakoid-membrane-bound APX in chloroplasts and showed increased tolerance to photooxidative stress, were used for evaluation of the relationship between H2O2 accumulation or change of redox status of PET and cAPX induction under photooxidative stress condition. There was no difference in the increase in the transcript level of cAPX in the first 1 h after irradiation with high-intensity light between the wild-type and either of the transgenic plants. The transcript level of cAPX in the wild-type showed a steady gradual increase during the next 5 h, while that in the transgenic plants during this period was stable. The H2O2 level of wild-type plants increased after 1 h, while those of transgenic plants remained constant. The decrease in q(p) value in all types of plants occurred earlier than the increase in H2O2 level. These results indicate that the induction of cAPX expression is caused by a redox change in PET, probably through the plastquinone pool at an early stage and thereafter by an increase in the cellular H2O2 level.