MUTATIONAL ANALYSIS OF RACE SPECIFIC RESISTANCE

植物育种家已经在野生植物中鉴定出抗性等位基因 分离并利用这些等位基因进行现代育种， 抗病品种 深入了解遗传基础 植物中的抗性和易感性可能为 建立人类疾病。 我们选择研究大麦的白粉病， 由专性子囊菌（Erysiphe graminis f.）sp. 霍代。 大麦- E。graminis相互作用的特点是 非常特殊 也就是说，一个给定的大麦品系对一种 特定的E.禾本科的种族，相反，一个给定的种族是 在有限的特定大麦品系上具有毒性。 一种广泛 在植物病理学文献中公认的假设，“基因- “for-基因”假说，表明最小数量的基因， 区分抗性和易感性的方法之一。 我们 初步数据表明，“基因对基因”假说确实 没有充分描述对E的种族特异性抗性。禾本科 大麦 在目前的研究中， 对特定E. Graminis比赛将由 突变分析 我们将筛选出一个突变群体， 抗性大麦幼苗的敏感突变体。 详细 易感株感染顺序的细胞学分析 大麦突变体将提供有关贡献的信息， 每种疾病反应基因建立不相容 关系和反抗的表达。 一旦基因 抗性的基础是充分了解克隆策略 可以设计抗性基因。 因此类 知识更合理的方法来发展 利用抗病性变异性的抗性大麦品种 现存于野生分离株中，在未来，变异性产生的 克隆的疾病反应基因的体外操作可以 进行。

Plant breeders have identified resistance alleles in wild plant isolates and have exploited these alleles in breeding modern, disease-resistant cultivars. Insight into the genetic basis of resistance and susceptibility in plants may provide models for the establishment of human diseases. We have chosen to study the powdery mildew disease of barley, caused by the obligate ascomycete, Erysiphe graminis f. sp. hordei. Barley - E. graminis interactions are characterized by extreme specificity. That is a given barley line is resistant to a specific set of E. graminis races, and conversely a given race is virulent on a limited, specific set of barley lines. A widely accepted hypothesis in the plant pathology literature, the "gene- for-gene" hypothesis, suggests that the minimum number of genes which distinguish resistance from susceptibility is one. Our preliminary data suggest that the "gene-for-gene" hypothesis does not adequately describe race-specific resistance to E. graminis in barley. In the present study the number of genes conditioning resistance to a specific E. graminis race will be determined by mutational analysis. We shall screen a mutagenized population of resistant barley seedlings for susceptible mutants. Detailed cytological analysis of the infection sequence of susceptible barley mutants will provide information about the contribution of each disease reaction gene to the establishment of incompatible relationships and the expression of resistance. Once the genetic basis of resistance is adequately understood strategies for cloning resistance genes can be devised. As a consequence of such knowledge more rational approaches to the development of resistant barley cultivars using variability in disease resistance extant in wild isolates, and in the future, variability generated by in vitro manipulation of cloned disease reaction genes may be undertaken.