| Project/Area Number |
61480047
|
|---|
| Research Category |
Grant-in-Aid for General Scientific Research (B)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
植物保護
|
|---|
| Research Institution | Tottori University |
|---|
Principal Investigator |
KODAMA Motoichiro Instru (1987-1988) Tottori University, Faculty of Agriculture, 農学部, 助手 (00183343)
尾谷 浩 (1986) 鳥取大, 農学部, 助教授 (50032305)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
OTANI Hiroshi Associate Tottori University, Faculty of Agriculture, 農学部, 助教授 (50032305)
KOHMOTO Keisuke Prof. Tottori University, Faculty of Agriculture, 農学部, 教授 (80032093)
児玉 基一朗 鳥取大学, 農学部, 助手 (00183343)
|
|---|
| Project Period (FY) |
1986 – 1988
|
| Project Status |
Completed (Fiscal Year 1988)
|
| Budget Amount *help |
¥5,700,000 (Direct Cost: ¥5,700,000)
Fiscal Year 1988: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1987: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 1986: ¥3,200,000 (Direct Cost: ¥3,200,000)
|
|---|
| Keywords | Host-specific toxin / Infection-inducing factor / 毒素受容体 / 感染誘発因子 / 細胞膜 / 葉緑体 / 毒素結合物質 / ミトコンドリア |
|---|
| Research Abstract |
Host-specific toxins (HSTs) from Alternaria spp can be classified into three groups in terms of primary action site. The first groups stands for HST which initially affects susceptible plasma membranes (e.g. AK-toxin). The second is HST which inhibits mitochondrial function (ACR toxin) and the third is HST whose primary targets locate on chloroplasts and plasma membranes (AM-toxin). Released toxins from spores can predispose host cells to be accessible to fungal ingress, which later leads to successful infection and eventual host cell death, regardless of their entirely differnt initial effects. In depth analysis of the action process of HSTs reveals that the toxin-induced accessibility process is definitely independent of the necrotic cell death process, except very early steps of toxin action from possible toxin-binding at the prime sites to modulation in plasma membrane function.
Continuous light irradiation to leaves after AM-toxin exposure inhibited toxin-induced necrosis on susceptible apple leaves. However, light did not affect toxin-induced electrolyte loss and reduction of photosynthetic CO_2 fixation. AK-toxin binding substances in susceptible plasma membranes were identified. ACR-toxin caused uncoupling of oxidative phosphorylation and changes in membrane potential in mitochondria from leaves of the susceptible host. ACR-toxin also inhibited malate oxidatio, apparently because of lack of NAD^+ in the matrix. The effects of the toxin on mitochondria from rough lemon were similar the effects of HMT-toxin on mitochondria from T-cytoplasm maize.
Infection-inducting factors produced by Botrytis sp. Cladosporium fulvum and Ophiostoma ulmi were isolated from spore-germinated fluids of each pathogen.
|
