小麦条锈病,由条锈病引起。小麦(PST),是最具破坏性的疾病之一,会在世界上许多地区造成严重的产量损失。由于小麦基因组的庞大和复杂,研究小麦与PST相互作用的分子机制是困难的。短枝矮子已成为温带草功能基因组学研究的模型系统。表型评估表明,短臂对PST的反应是非宿主抗性(NHR),这使我们能够将这种植物-病原体系统作为模型来探索小麦和PST的免疫反应以及潜在的分子机制。在这里,我们报道了基于高效农杆菌介导的转化系统的约7,000个T-DNA插入系的产生。获得了数百种比野生型Bd21更易感或更耐PST的突变体。三个推定的靶基因,三个T-DNA插入突变体的Bradi5g17540,BdMYB102和Bradi5g11590可能参与了小麦条锈病的短枝硬茎的NHR。这种T-DNA突变体的系统病理研究将拓宽我们对NHR的认识,并协助培育具有持久抗性的小麦品种。
Wheat stripe rust, caused by Puccinia striiformis f. sp. tritici (PST), is one of the most destructive diseases and can cause severe yield losses in many regions of the world. Because of the large size and complexity of wheat genome, it is difficult to
study the molecular mechanism of interaction between wheat and PST. Brachypodium distachyon has become a model system for temperate grasses\' functional genomics research. The phenotypic evaluation showed that the response of Brachypodium distachyon to PST was nonhost resistance (NHR), which allowed us to present this plant-pathogen system as a model to explore the immune response and the molecular mechanism underlying wheat and PST. Here we reported the generation of about 7,000 T-DNA insertion lines based on a highly efficient Agrobacterium-mediated transformation system. Hundreds of mutants either more susceptible or more resistant to PST than that of the wild type Bd21 were obtained. The three putative target genes, Bradi5g17540, BdMYB102 and Bradi5g11590, of three T-DNA insertion mutants could be involved in NHR of Brachypodium distachyon to wheat stripe rust. The systemic pathologic
study of this T-DNA mutants would broaden our knowledge of NHR, and assist in breeding wheat cultivars with durable resistance.