Molecular dissection of plant defense responses to necrotrophic pathogens

由坏死性病原体引起的植物疾病每年造成高达数百万美元的损失。坏死性真菌在定植前主动杀死宿主组织，通常通过分泌毒素来杀死宿主组织。这与生物营养型病原体不同，后者需要活的宿主细胞来完成它们的生命周期。最普遍和最具破坏性的坏死菌之一是灰霉病菌，它是一种真菌病原体，在许多植物物种中引起各种收获前和收获后的疾病。预防灰霉病的主要手段是化学防治疾病；然而，由于病原菌中出现了对杀菌剂的抗药性，以及消费者对产品和环境中残留活性的担忧，这一方法受到了严重阻碍。遗传抗性将是最可取的，但目前它是有限的，因为缺乏关于寄主对灰霉病抗性的基因和机制的信息。本项目的目标是深入了解在对灰霉病的防御反应中起关键作用的分子和细胞因素。通过基因和基因组方法的结合，已经发现了许多控制寄主对病原体反应的基因座。其中BOS1(Botrytis Sensible 1)被分离出来，并编码一个R2R3MYB转录因子，该转录因子是限制灰霉病在受感染植物中生长所必需的。这一建议试图通过确定BOS1影响或调节哪些基因和途径来调节拟南芥防御反应的一个重要的、相对较少被理解的臂来阐明BOS1的功能。这一建议可能会极大地增加我们对植物如何识别和响应灰霉病和其他坏死性真菌攻击的理解，为这一领域的未来进展开辟道路。更好地了解植物与坏死性病原体抗争的基因和机制，将揭示管理由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灰霉病品种的选育，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，该项目将提供充足的机会，让各级教育的学生参与和培训遗传学、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.