Abstract
Light-dependent activation of the tryptamine pathway in Sekiguchi lesion (sl) mutants (Sekiguchi-asahi, Sekiguchi-koshihikari, and Sekiguchi-sasanishiki) inoculated with Magnaporthe grisea, was demonstrated by a significant increase in tryptophan decarboxylase and monoamine oxidase activities and tryptamine accumulation. Terminal deoxynucleotidyl transferase-mediated dUTP-nick end labeling (TUNEL) staining and gel analysis indicated DNA fragmentation in cells of leaf tissues with Sekiguchi lesions of the three sl mutants. Furthermore, increased DNase activity was also light-dependent in the sl mutants after inoculation with M. grisea. DNA fragmentation was inhibited in leaves when Sekiguchi lesion formation was suppressed by cycloheximide and heat shock pretreatments. These data suggest that Sekiguchi lesion formation in the sl mutants is an apoptosis-like response and that its response is induced by light-dependent activation of the tryptamine pathway, which is responsible for light-enhanced resistance.
Published Version
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