Molecular dissection of plant defense responses to necrotrophic pathogens

由坏死营养型病原体引起的植物病害每年造成数百万美元的损失。 坏死性真菌在定植前通常通过分泌毒素主动杀死宿主组织。 这与需要活的宿主细胞来完成其生命周期的活体营养型病原体形成对比。 最普遍和最具破坏性的坏死营养菌之一是灰葡萄孢菌（Botrytis cinerea），这是一种真菌病原体，其在许多植物物种中引起多种收获前和收获后疾病。 预防葡萄孢属的主要手段是化学病害防治;然而，由于病原体中杀菌剂抗性的出现以及消费者对产品和环境中残留活性的担忧，化学病害防治受到严重阻碍。遗传抗性将是最理想的，但目前它是有限的，因为缺乏信息的基因和机制的基础上，寄主抗Botrytis。本项目的目标是深入了解的分子和细胞因子，在防御反应中发挥关键作用的葡萄孢。 通过遗传学和基因组学方法的结合，已经发现了许多控制宿主对病原体反应的基因座。 其中之一，BOS 1（Botrytis susceptible 1），被分离并编码限制感染植物中的Botrytis生长所需的R2 R3 MYB转录因子。 该提案旨在通过确定BOS 1影响或调节哪些基因和途径来阐明BOS 1的功能，以调节拟南芥防御反应的一个重要且相对较少了解的分支。这一提议可能会极大地增加我们对植物如何识别和应对葡萄孢菌和其他坏死性真菌攻击的理解，为该领域的未来发展开辟道路。 更好地了解植物与坏死营养型病原体竞争的基因和机制将揭示管理此类病原体引起的疾病的新的有效方法。 这些知识将有助于指导抗葡萄孢品种的培育，以实现安全和可持续的作物保护。 最终，公共安全和环境质量将得到提高。 此外，该项目将提供充分的机会，让各级教育的学生参与和培训遗传、分子和植物病理学研究的原理和应用，并加强教育的多样性。

Plant diseases caused by necrotrophic pathogens result in losses amounting to millions of dollars a year. Necrotrophic fungi actively kill host tissue prior to colonization usually through the secretion of toxins. This is in contrast to biotrophic pathogens that require living host cells to complete their life cycle. One of the most prevalent and damaging necrotrophs is Botrytis cinerea, a fungal pathogen which causes a variety of pre- and post-harvest diseases in a number of plant species. The principal means of protection against Botrytis is chemical disease control; however, it is seriously hampered by the emergence of fungicide resistance in the pathogen and consumer concern over residual activity in the produce and in the environment. Genetic resistance would be most desirable, but at present it is limited because of paucity of information on genes and mechanisms that underlie host resistance to Botrytis.The goal of this project is to gain insight into the molecular and cellular factors that play a crucial role in defense responses to Botrytis. Through a combination of genetic and genomic approaches many loci that control host response to the pathogen have been uncovered. One of these, BOS1 (Botrytis susceptible 1), was isolated and encodes an R2R3MYB transcription factor required for restricting Botrytis growth in infected plants. This proposal seeks to elucidate the function of BOS1 by determining what genes and pathways it impacts or modulates to regulate an important and relatively less understood arm of the Arabidopsis defense response. This proposal is likely to add tremendously to our understanding of how plants recognize and respond to attack by Botrytis and other necrotrophic fungi, opening the way for future advances in this area. A better appreciation of genes and mechanisms by which plants contend with necrotrophic pathogens will reveal new and effective ways for managing diseases caused by such pathogens. Such knowledge will help direct the breeding of Botrytis resistant cultivars for safe and sustainable crop protection. Ultimately, public safety and environmental quality will be enhanced. In addition, this project will provide ample opportunities for engaging and training students at all levels of education in the principles and applications of genetic, molecular, and plant pathology research, and for enhancing diversity in education.