Cellular and molecular biology of verticillium diseases

轮枝菌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的作物中造成重大的经济损失。 我们的研究项目是一个长期的项目，重点是番茄黄萎病抗性和致病相关的细胞和分子机制。 在该病理系统中，抗性通常与宿主中低水平的真菌定殖和最小的症状表达相关，而易感性与导致植物疾病和死亡的高水平定殖相关。 然而，可以发生耐受性相互作用，其中无毒病原体感染的水平与相容性相互作用相似，但很少或没有疾病发展。 事实上，寄主植物甚至比未受感染的植物更高，更健壮，甚至可以保护番茄免受更毒的轮枝菌属小种的侵害。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性。 然而，传统的育种方法已经有点无效，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，但目前受到缺乏有关控制轮枝菌属的抗性，耐受性和易感性的分子机制的信息。 在这里，我们提出了以下问题：1）是否有不同的基因表达模式，表征和作为抗性，易感性和耐受性的遗传指纹，如果有的话，是什么基因？2)哪些下游基因受到Ve 1和/或Ve 2基因沉默或过度表达的影响，这些基因提供了对真菌强毒株的抗性，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)在番茄植株中， （Dvd-E6）和强毒（Vd 1）分离株，是否有Dvd-E6和宿主之间的遗传相互作用，可以解释对Vd 1的保护？如果是这样的话，番茄的基因是什么？ 最终目标是通过基因工程培育更健康的作物，这对农民和消费者都有利。

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.