Phytophthora infestans effector PexRD54 associates with host Rab GTPase Rab8-1 to reprogram endomembrane transport

丝状植物病原体是一组真核病原体，包括卵菌属疫霉，以及锈菌、白粉菌等，它们是最具破坏性的植物病害，威胁着全球粮食安全。这些病原体每年给现代农业造成数十亿美元的损失，并严重影响发展中国家的自给农业。这些微生物通过专门的细胞结构被安置在宿主细胞内。然而，对植物细胞内微生物调节的分子机制知之甚少。本研究旨在描述丝状植物病原体在植物细胞内调节所需的寄主过程，并特别关注植物膜运输系统在这一过程中的作用。在卵菌中，疫霉（Phytophthora spp.）引起了世界上一些最具破坏性的植物病害，对马铃薯、番茄、大豆等重要作物物种造成巨大的经济损失，并对自然生态系统造成环境破坏。引起马铃薯和番茄晚疫病的爱尔兰马铃薯饥荒病原体疫霉（Phytophthora infestans）是全球粮食生产最重要的生物威胁之一，每年导致全球经济损失超过50亿美元。不幸的是，马铃薯晚疫病是一种重新出现的破坏性疾病，最近在英国各地的马铃薯农场造成了严重的流行病。我们的长期目标是剖析植物细胞自主免疫的分子机制，并通过特别使用P. infestans作为模型病原体来研究细胞膜运输在这一过程中的作用。像其他一些形成破坏性植物疾病的丝状病原体一样，假单胞杆菌通过形成称为吸器的特殊隔室被安置在宿主细胞内，吸器通过新合成的来源和成分未知的宿主衍生膜与入侵的植物细胞分离。该界面通过实现高效的大分子交换，对寄生虫感染的发展至关重要。因此，了解寄主与病原菌界面上大分子交换过程的调控对于开发新的植物抗病工程策略至关重要。不幸的是，尽管几十年前就发现了吸器，但我们目前对吸器的了解有限。破译这个界面的细胞和生化活动对于理解发病机制至关重要。像其他病原体一样，P. infestans分泌一组蛋白质，称为效应物，抑制植物免疫并使寄生虫感染。最近，我们发现这些效应物中的一些在被感染的植物细胞内特异性地积聚在宿主病原体界面上。在这项研究中，我们的目的是利用一种称为perrd54的效应物作为分子探针来鉴定局灶免疫的宿主成分。我们的初步工作揭示了在吸器周围，perrd54与宿主蛋白Rab8-1相关，Rab8-1是真核生物囊泡运输调节因子Rab GTPases家族的成员。我们的目标是对PexRD54和Rab8-1进行功能表征，以确定这些分子在宿主病原体界面上的作用。这项研究将有助于建立受病原体干扰的植物膜运输过程的功能特征，并有助于了解宿主病原体界面的起源、功能和组成。反过来，对perrd54操纵Rab8-1的详细了解将提高我们对植物细胞内微生物调节的理解，并将为作物的抗病工程创造新的机会。

Filamentous plant pathogens are a group of eukaryotic pathogens including oomycete genus Phytophthora, as well as rust fungi, and Powdery mildew fungi, which cause most destructive plant diseases and threaten global food security. These pathogens cost billions of dollars annual looses to modern agriculture and severely impact subsistence agriculture in developing countries. These microorganisms are accommodated within the host cells through specialized cellular structures. However, little is known about molecular mechanisms underlying microbial accommodation inside the plant cells. The proposed research aims to characterize the host processes required for accommodation of filamentous plant pathogens inside the plant cells with a specific focus on illustrating the role of plant endomembrane transport system in this process. Among the oomycetes, Phytophthora spp. cause some of the most destructive plant diseases in the world and cause enormous economic damage to important crop species such as potato, tomato, and soybean, as well as environmental damage in natural ecosystems. Phytophthora infestans, the Irish potato famine pathogen, which causes late blight of potato and tomato, is one of the most important biotic threats to global food production leading to worldwide economic losses exceeding $5 billion annually. Unfortunately, late blight of potato is a reemerging destructive disease, which caused severe epidemics in potato farms across the UK lately. Our long-term objective is to dissect the molecular mechanisms underlying plant cell autonomous immunity and the role of endomembrane traffic in this process by particularly using P. infestans as a model pathogen. Like some other filamentous pathogens that form destructive plant diseases, P. infestans is accommodated inside the host cells by forming specialized compartments termed haustoria, which are separated from the invaded plant cells by newly synthesized host derived membranes with unknown origin and composition. This interface is critical for development of parasitic infection by enabling efficient macromolecule exchange. Therefore, understanding the regulation of macromolecule exchange processes at host pathogen interface is critical to develop novel strategies to engineer disease resistance in plants. Unfortunately, despite being discovered decades ago, our current knowledge about haustoria is limited. Deciphering the cellular and biochemical activities at this interface is critical for understanding the mechanisms of pathogenesis. Like other pathogens, P. infestans secretes a battery of proteins, termed effectors that suppress plant immunity and enable parasitic infection. Recently we discovered that some of these effectors specifically accumulate at the host pathogen interface inside the infected plant cells. In this study we aimed to identify host components of focal immunity using one such effector, termed PexRD54, as a molecular probe. Our preliminary work unraveled that around haustoria, PexRD54 associated with a host protein named Rab8-1, a member of Rab GTPases family of eukaryotic vesicle trafficking regulators. Our goal is to functionally characterize PexRD54 and Rab8-1 in order to establish the roles of these molecules at host pathogen interface. This study will help to establish functional characterization of plant endomembrane transport processes perturbed by pathogens and help understanding the origin, function and composition of the host pathogen interface. In turn, a detailed knowledge of PexRD54 manipulation of Rab8-1 will improve our understanding of the microbial accommodation inside the plant cells and will allow for creating renewed opportunities for engineering disease resistance in crops.