| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2006: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2005: ¥2,500,000 (Direct Cost: ¥2,500,000)
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| Research Abstract |
A lesion-mimic mutant of rice (cv. Sekiguchi-asahi) showed enhanced resistance to Magnaporthe grisea infection, thereby inducing Sekiguchi lesion (sl) formation and tryptamine accumulation under light. Spontaneous Sekiguchi lesions were induced in green tissues with chloroplasts, but not in albino tissues without chloroplasts. Both Sekiguchi lesion formation and tryptamine accumulation in leaves infected with M. grisea were inhibited by pre-treatment with the photosynthetic inhibitor, 3-(3,4-dicchlorophenyl)-1,1-dimethylurea (DCMU), which suppressed the gene expression of tryptophan decarboxylase, monoamine oxidase activity, H_2O_2 generation and DNA fragmentation. Chloroplasts appear to be the key mediators of cell death in the sl mutant. Catalase activity was significantly inhibited by M. grisea infection under light, but maintained a high level in leaves pretreated with DCMU. The propagative nature of light-dependent Sekiguchi lesions suggests that tryptamine-mediated cell death is caused by a diffusible agent such as hydrogen peroxide. Furthermore, tryptophan accumulated in M. grisea-infected leaves under light, but not in DCMU-pretreated ones. Such DCMU inhibition of tryptamine pathway-mediated cell death disappeared in the presence of exogenous tryptophan, suggesting a strong correlation between light-dependent tryptamine accumulation and the activation of the tryptophan biosynthetic pathway after M. grisea infection.
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