2006 Fiscal Year Final Research Report Summary
Molecular elucidation of tryptamine-pathway mediated hypersensitive cell death in lesion mimic mutants of rice infected with Magnaporthe grisea
| Project/Area Number |
17580039
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Plant pathology
|
|---|
| Research Institution | Shimane University |
|---|
Principal Investigator |
ARASE Sakae Shimane University, Life and Environmental Science, Professor, 生物資源科学部, 教授 (40127478)
|
|---|
| Project Period (FY) |
2005 – 2006
|
| Keywords | tryptophan decarboxylase / monoamine oxidase / Sekiguchi lesion / rice blast / lesion mimic mutant / tryptamine / catalase / photo-synthesis |
|---|
| 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.
|
