| Project/Area Number |
17580001
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Breeding science
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| Research Institution | HOKKAIDO UNIVERSITY |
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Principal Investigator |
INUKAI Tsuyoshi Hokkaido Univ. Research Faculty of Agriculture, Assis.Prof., 大学院農学研究院, 助手 (90223239)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2006: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2005: ¥2,400,000 (Direct Cost: ¥2,400,000)
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| Keywords | Arabidopsis / Turnip mosaic virus / Necrosis / アラビドプシス |
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| Research Abstract |
In the pathosystems of Turnip mosaic virus (TuMV) and Brassica crops, various symptoms are developed such as mosaic and necrosis leading to loss of yield and product quality. Although necrotic symptom causes more severe damage in plants infected by TuMV, the induction mechanism of necrosis is poorly understood so far. We previously identified the symptom determinant TuNI in Arabidopsis thaliana, a model species of the family Brassicaceae. The TuNI gene directly or indirectly interacts to a TuMV factor and induces veinal necrosis in Arabidopsis. In this study it was shown that the necrotic symptom induced by TuNI was a form of defense responses accompanying with HR-like cell death along veins even though the systemic infection finally leaded to plant death. The necrotic symptom is occurred along veins in response to the spread of TuMV and the virus is often localized in the necrotic region. The necrotic response is associated with occurrence of H_2O_2 along veins, accumulation of salicylic acid (SA) and expression of defense genes. Additionally, this HR-like cell death with defense gene expression is weakened or disappeared by light shading treatment. These features are similar to resistance reaction to pathogens. However, the induction of necrosis is mediated by three phytohormones SA, jasmonic acid (JA) and ethylene, and both SA・ dependent and JA/ethylene-dependent PR genes are activated. These results reveled that veinal necrosis induced by TuMV infection was regulated by a complex network of signaling pathways which is different from that of resistance reaction.
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