Cellular and molecular biology of verticillium diseases

黄萎病是一种重要的植物病原菌。每年，枯萎病在全世界数百种不同作物中造成重大经济损失。我们的研究计划是长期的，重点研究番茄黄萎病的细胞和分子抗性机制和发病机制。在这种病理系统中，抗性通常与低水平的真菌定植和宿主的最小症状表达有关，而易感性与高水平的定植导致植物病害和死亡有关。然而，耐受相互作用可以发生，其中无毒病原体感染水平与兼容相互作用相似，但很少或没有疾病发展。事实上，寄主植物甚至比未感染的植物更高、更健壮，甚至可以保护西红柿免受更毒的黄萎病种的侵害。然而，这可能导致病原体在田间积聚。最好的控制方法是培育抗药性。然而，传统的育种方法有些无效，因为在大多数宿主中，抗性是多基因的，难以处理。生物技术提供了更多的希望，但目前由于缺乏控制黄萎病抗性、耐受性和易感性的分子机制的信息而受到阻碍。在这里，我们提出以下问题：1)是否存在不同的基因表达模式，作为抗性、易感性和耐受性的遗传指纹，如果有，这些基因是什么？2)哪些下游基因受到沉默或过表达Ve1和/或Ve2基因的影响，这些基因提供了对真菌毒力菌株的抗性，其生物学后果是什么？3)还有哪些基因对抗性、易感性和耐受性至关重要？4)在被无毒（Dvd-E6）和有毒（Vd1）分离株定殖的番茄植株中，Dvd-E6和宿主之间是否存在遗传相互作用，可以解释对Vd1的保护？如果是这样，那么涉及到哪些番茄基因呢？最终目标是培育更健康的转基因作物，这对农民和消费者都有好处。

Verticillium is an important plant pathogen. Each year wilt diseases cause major economic losses in hundreds of different crops worldwide. Our research program is a long-term one, focusing on the cellular and molecular mechanisms of resistance and pathogenesis associated with verticillium wilt disease of tomato. In this pathosystem resistance is usually associated with low levels of fungal colonization and minimal symptom expression in the host and susceptibility with high levels of colonization resulting in plant disease and death. However, tolerant interactions can occur in which the levels of avirulent pathogen infection are similar to compatible interactions but little or no disease develops. In fact, host plants are taller and more robust than even uninfected plants and can even protect tomatoes from more virulent races of Verticillium. However, this can lead to pathogen buildup in fields. The best method of control is breeding for resistance. However, traditional breeding approaches have been somewhat ineffective since, in most hosts, resistance is polygenic and difficult to work with. Biotechnology offers more promise but is currently hampered by lack of information about the molecular mechanisms controlling resistance, tolerance and susceptibility to Verticillium spp. Here we ask the following questions: 1) Are there distinct gene expression patterns that characterize and act as genetic fingerprints of resistance, susceptibility and tolerance and, if so, what are the genes? 2) What downstream genes are affected by the silencing or over expression of the Ve1 and/or Ve2 genes that provide resistance against virulent strains of the fungus and what are the biological consequences? 3) What other genes are critical to resistance, susceptibility and tolerance? 4) In tomato plants colonized by both avirulent (Dvd-E6) and virulent (Vd1) isolates, is there genetic interplay between Dvd-E6 and the host that could explain protection against Vd1? If so, what tomato genes are involved? The end goal is to genetically engineer healthier crops, which would be of benefit to both farmers and consumers.