Sekiguchi lesion (sl) mutant of rice infected with Magnaporthe grisea showed enhanced resistance under light inducing the Sekiguchi lesion formation and tryptamine accumulation. In M. grisea-infected leaves, high level of tryptophan decarboxylase (TDC) and monoamine oxidase (MAO) activities were light-dependently maintained. When the M. grisea-inoculated leaves were irradiated by band-pass filter (BPF)-filtered lights from daylight fluorescent lamps, Sekiguchi lesion development, tryptamine accumulation and TDC and MAO activities were enhanced by increasing the wavelength of visible　light. DNA fragmentation occurred in cells of leaf tissues with Sekiguchi lesion of the sl mutants. The suppressive and inducible effects of biotic and abiotic agents on the induction of DNA fragmentation in the leaves of the sl mutant agree well with those effects on the activation of the tryptamine pathway involved in Sekiguchi lesion formation. Glyphosate [N-(phosphonomethyl) glycine] and DCMU [3-(3,4-dichlorophenyl)-1,1-dimethylurea] pretreatments suppressed Sekiguchi lesion formation, DNA fragmentation and tryptamine accumulation in the sl mutant after M. grisea infection even under light. This inhibition by two chemicals was blocked by the supply of exogenous tryptophan, but not by exogenous phenylalanine. During tryptophan starvation, catalase activity was maintained at a high level even under light, leading to the suppression of H₂O₂ generation and DNA fragmentation. These data show a strong relationship between the tryptophan and tryptamine pathways in the induction of light-enhanced resistance to M. grisea infection in the sl mutant.