Analysis of Molecular Basis for Gene-for-Gene Complementarity in Plant Diseases : Isolation of an Avirulence Gene from Phytophthora megasperma

在特定的小种和植物品种之间的特定组合中的疾病专一性被称为“小种-品种专一性”。这种疾病的专一性通常由基因对基因的互补性控制，即只有当表达显性抗病基因的植物品种受到表达互补致病基因的病原菌小种的攻击时，才会发生抗性反应。大豆(Glyine Max)与植物疫霉病菌(Phytophthora measperma f.sp.gicinea)的相互作用是目前最清楚的植物病原菌基因对基因系统之一，在该系统中植物抗病蛋白的产生过程已被分析。该真菌的菌丝壁已被证明是有效的乙醇胺积累的诱导子，它们可能在诱导感染植物中植物保卫素的积累中发挥作用。然而，目前还没有分离到解释大豆品种与大孢霉小种之间的特异性的特异性激发子，也没有分离到该真菌的无毒基因。因此，我们在本研究中试图分离出一个无毒基因。不幸的是，我们未能实现我们的最终目标：从大精粉病菌中分离出一个无毒基因。然而，我们可以揭示在感染P.measperma rase1的大豆叶片(Harosoy)的胞间液中存在潜在的特异性激发子，以解释该真菌与植物之间的特异性。此外，我们还可以展示一个结构模型，说明葡聚糖激发子最初是如何存在于P.measperma的细胞壁中并由宿主β-1，3-内切葡聚糖酶释放的；这些数据已发表在《植物生理学》(1995)上。此外，我们还可以从大豆根细胞的膜部分中纯化葡聚糖激发子结合蛋白，并分离出它的cDNA；这些数据已经发表在Proc.Natl.Academy.Science美国期刊(1997，出版社)上。

Disease specificity in a particular combination between a given race and a plant cultivar is called as "race-cultivar specificity". This disease specificity is frequently controlled by gene-for-gene complementarity, in which resistance responses occur only when plant cultivars that express a dominant resistance gene are attacked by pathogen races that express a complementary a virulence gene. The interaction between soybean (Glycine max) and the fungal pathogen Phytophthora megasperma f.sp.glycinea is one of the best understood gene-for-gene plant-pathogen systems in which the processes leading to production of the phytoalexin glyceollin have been analyzed. Mycelial walls of the fungus have been shown to be potent elicitors of glyceollin accumulation, and their possible role in the induction of phytoalexin accumulation in infected plants has been suggested. However, neither specific elicitor explaining specificity between a soybean-cultivar and a race of P.megasperma nor avirulence gene of the fungus has been isolated. Thus, we have tried to isolate an avirulence gene of P.megasperma in this study. Unfortunately, we failed to achieve our final object : to isolate an avirulence gene from P.megasperma. However, we could reveal the existence of potential specific elicitor in intercellular fluid from P.megasperma rase1 infected soybean leaves (cv.Harosoy) to explain a specificity between the fungus and the plant. And also, we could show a structural model of how glucan elicitor is originally present in cell walls of P.megasperma and released by host beta-1,3-endoglucanase ; these data have been published in Plant Physiology (1995). Moreover, we could purify a glucan elicitor-binding protein from the membrane fraction of soybean root cells, and isolate its cDNA ; these data have been published in Proc.Natl.Acad.Sci.USA (1997, in press).