Cellular and molecular biology of verticillium diseases

黄萎病的细胞和分子生物学

• 批准号: 2961-2010
• 负责人: Robb, Jane
• 金额: $ 1.97万
• 依托单位: University of Guelph
• 依托单位国家: 加拿大
• 项目类别: Discovery Grants Program - Individual
• 财政年份: 2012
• 资助国家: 加拿大
• 起止时间: 2012-01-01 至 2013-12-31
• 项目状态: 已结题
• 来源: https://www.nserc-crsng.gc.ca/ase-oro/Details-Detailles_eng.asp?id=506393
• 关键词: Cellular; molecular; biology; verticillium; diseases

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.

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的农作物上造成重大经济损失。我们的研究计划是长期的，重点是与番茄黄萎病相关的抗性和发病机制的细胞和分子机制。在这一病理系统中，抗性通常与真菌在寄主中的低水平定植和最低程度的症状表达有关，而与高定殖水平的敏感性有关，从而导致植物病害和死亡。然而，可以发生耐受性相互作用，其中无毒病原体感染水平类似于相容相互作用，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强的黄萎病小种的侵袭。然而，这可能会导致病原菌在田间积聚。最好的防治方法是进行抗病育种。然而，传统的育种方法在某种程度上是无效的，因为在大多数宿主中，抗性是多基因的，很难处理。生物技术提供了更多的希望，但目前由于缺乏关于控制黄萎病抗性、耐受性和敏感性的分子机制的信息而受到阻碍。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来表征和充当抗性、敏感性和耐受性的遗传指纹？如果有，哪些基因是？2)Ve1和/或Ve2基因的沉默或过度表达会影响哪些下游基因，从而提供对该真菌强毒力菌株的抗性，其生物学后果是什么？3)哪些其他基因对抗性、敏感性和耐性至关重要？4)在被无毒(DVD-E6)和强毒(Vd1)分离物侵染的番茄植株中，DVD-E6和寄主之间是否存在基因相互作用，以解释对Vd1的保护？如果是这样的话，哪些番茄基因参与其中？最终目标是通过基因工程获得更健康的作物，这将使农民和消费者都受益。