Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2004: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2003: ¥2,700,000 (Direct Cost: ¥2,700,000)
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Research Abstract |
Increased tryptohan decarboxylase(TDC) and monoamine oxidase(MAO) activities were observed in Sekiguchi lesion mutant infected with Mgrisea. These enzyme activities were observed before the penetration of M. grisea to rice cells and maintained high levels even after Sekiguchi lesion formation. Light-dependent expression of TDC gene was observed in leaves inoculated with M.grisea before Sekiguchi lesion formation. Spore germination fluid of M grisea also induced Sekiguchi lesion formation accompanied by increased enzymes activities and tryptamine accumulation. Sekiguchi lesion was also induced by treatments with substrates for MAO under light, but not induced by non-substrates under light. Light-dependent induction of Sekiguchi lesion by tryptamine was significantly inhibited in the presence of MAO inhibitors and H_2O_2-scavengers. In cycloheximide(CHX)- or heat (HS)-pre-treated leaves of the Sekiguchi lesion mutant, the formation of Sekiguchi lesions and the accumulation of tryptamine
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by M.grisea infection were significantly inhibited. In the CHX- or HS-pre-treated leaves, light-dependent induction of both TDC and MAO activities was also significantly inhibited. DNA fragmentation and DNase activity were significantly induced in leaves of the Sekiguchi lesion mutant inoculated with M.grisea under light. In the CHX- or HS-pre-treated leaves, however, neither laddering nor DNase activity was observed even under light. Terminal deoxynucleotidyl transferase-mediated dUTP-nic end labeling staining and gel analysis indicated DNA fragmentation in cells of leaf tissues with Sekiguchi lesions. These data show that : 1)Tryptamine pathway in the Sekiguchi lesion mutants is activated by light of long wavelength, 2)Catalase activity is inhibited by light irradiation of long wavelengths (550-650nm) in sekiguchi lesion mutant inoculated with M. grisea, and tryptamine pathway was activated by H_2O_2 generation and accumulation, 3)Sekiguchi lesion formation in the Sekiguchi lesion 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. Less
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