| Summary: | 碩士 === 國立臺灣大學 === 植物病理與微生物學研究所 === 106 === Neutralized phosphorous acid (NPA) is widely used for the management of plant diseases caused by oomycete pathogens including Phytophthora parasitica. While it has been proposed that phosphonate, the effective component of NPA, may function through enhancing plant resistance, the detailed mechanism remains to be elucidated. To identify genes which might play key roles in NPA-induced resistance, microarray analysis was performed. The results showed that various genes are differentially expressed in NPA- and water-pretreated (as a control) tomato plants in response to infection by P. parasitica, with many of them involved in primary metabolisms, such as degradation of carbohydrates, amino acids, and fatty acids. In addition, following pathogen infection, genes involved in lipid metabolism were identified only in NPA-pretreated plants, which suggests their involvement in NPA-induced resistance. As well, autophagy-related genes including Atg3, Atg6, and Atg18 (a homolog of Arabidopsis thalianaAtg18b) were significantly upregulated in NPA-pretreated tomato plants as shown by microarray data. However, analysis by qRT-PCR indicated that these genes are upregulated only in the control but not NPA-pretreated plants. Examination by confocal microscopy of the subcellular distribution of Atg8-2-GFP, a potato Atg8CL homolog encoding a key protein of the autophagosome, demonstrated that infection by P. parasitica induced in Nicotiana benthamiana epidermal cells the formation of abundant autophagosomes, which are significantly reduced in NPA-pretreated plants. Tobacco rattle virus-mediated gene silencing of Atg3, Atg6, Atg8-2, and Atg18 did not alter tomato susceptibility towards the pathogen regardless of NPA treatment. However, downregulation of Atg8-4 did enhance disease symptom in the NPA-treated plants. These results suggest an important role of primary metabolism in plant response towards infection of P. parasitica, as well as a role of lipid metabolism and Atg8-4 in NPA-induced resistance.
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