A functional genomics approach to address the molecular evolutionary concept of pathogen host range and non-host resistance

植物先天免疫系统响应入侵病原体的一个主要分支依赖于通过模式识别受体（PRR）感知不变的微生物结构，通常称为微生物或病原体相关分子模式（MAMP/PAMP），随后激活通用抗微生物应答。这一过程统称为MAMP/PAMP触发免疫（MTI/PTI），保护植物免受大多数病原体的侵害，并反映了基础或非宿主抗性。成功的病原体已经进化出操纵或抑制MTI的效应子。连接宿主适应、宿主范围和非宿主抗性的分子进化概念规定，不能抑制MTI可能是由于缺乏能够有效干扰MAMP信号传导的效应物，最有可能是因为它们不能与宿主靶蛋白相互作用并正确操纵宿主靶蛋白。然而，很少有实验证据支持或证实这一概念。卵菌属疫霉是一个很好的模型来解决这些问题。它包含分类学上密切相关的物种，但显示不同的宿主范围特异性。本项目的总体目标将包括对来自不同疫霉属的MTI抑制RXLR效应物进行比较功能研究。在寄主和非寄主植物中。病原体物种形成，宿主适应和非宿主抗性现象在分子水平上的调查将提供深入了解卵菌基因组的可塑性，揭示了进化的保守性或多样化的RXLR效应，主机施加的正选择驱动。这种方法将有助于合理化和模拟病原体与宿主的共同进化，无论是密切（主机范围扩大）或遥远（主机跳跃）有关的本主机。

A major branch of the plant innate immune system in response to invading pathogens relies on the perception of invariant microbial structures, commonly termed Microbial- or Pathogen-Associated Molecular Patterns (MAMPs/PAMPs) by pattern recognition receptors (PRRs), followed by the activation of a generic anti-microbial response. This process, collectively termed MAMP/PAMP-triggered immunity (MTI/PTI), protects plants against the majority of pathogens and reflects basal or non-host resistance. Successful pathogens have evolved effectors that manipulate or suppress MTI. The molecular evolutionary concept connecting host adaptation, host range and non-host resistance stipulates that a failure to suppress MTI may be due to the lack of effectors capable to interfere efficiently with MAMP signalling, most likely because they are unable to interact with and properly manipulate host target proteins. However, there are very little experimental evidence supporting or infirming this concept.The oomycete genus Phytophthora is an excellent model to address these questions. It contains taxonomically closely-related species but displaying different host range specificities. The general objective of this project will consist to perform a comparative functional study of MTI-suppressing RXLR effectors originated from different Phytophthora spp. in host and non-host plant species. The investigation of pathogen speciation, host adaptation and the phenomenon of non-host resistance at the molecular level will offer insights into the plasticity of oomycete genomes, shedding light on the evolutionary conservation or diversification of RXLR effectors, driven by host-imposed positive selection. This approach will be instrumental to rationalize and to model pathogen co-evolution with hosts that are either closely (host range expansion) or distantly (host jump) related to the present hosts.