MUTATIONAL ANALYSIS OF RACE SPECIFIC RESISTANCE

植物育种者已经在野生植物中发现了抗性等位基因 并利用这些等位基因培育现代、 抗病品种。对遗传基础的洞察 植物中的抗性和敏感性可能为 人类疾病的建立。 我们选择研究大麦的白粉病， 由专性子囊菌Erysihe graminis f.sp. 霍尔代伊。大麦与禾本科真菌的相互作用的特征是 极端的专一性。也就是说，一个给定的大麦品系对 一组特定的小麦赤霉菌小种，相反，一个给定的小种是 在一组有限的、特定的大麦品系上致病。广为流传 植物病理学文献中公认的假说，“基因-- For-gene“假说，认为基因的最小数量 这是区分抗性和敏感性的一个原因。我们的 初步数据显示，“基因换基因”假说确实存在。 没有充分描述对小麦赤霉病的小种特异性抗性 大麦。在本研究中，基因条件化的数量 对特定的稻瘟病菌小种的抗性将由以下因素决定 突变分析。我们将筛选出一个诱变种群 感病突变体的抗性大麦幼苗。详细 易感人群感染序列的细胞学分析 大麦突变体将提供有关 每个疾病反应基因对建立不亲和性 关系和抵抗的表达。一旦遗传基因 抗药性的基础是充分了解克隆策略 抗性基因是可以设计出来的。由于这样的结果 知识发展的更理性途径 利用抗病变异性的大麦抗病品种 在野生分离物中的现存，以及在未来，由 克隆的疾病反应基因的体外操作可能是 承担了。

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.