Molecular analysis of apoplastic effector-mediated suppression of PTI signaling

通过膜结合的模式识别受体(PRRs)介导的植物天然免疫对于抵御微生物感染具有重要作用。然而，寄主适应的植物病原真菌和卵菌已经进化出质外体效应器，操纵植物的胞外功能以建立感染。最近，我们从寄主范围广泛的真菌病原菌大丽轮枝菌中分离到一个保守的效应蛋白SCP8。SCP8通过激活LRR-RK和LRR-RP型PRRs抑制拟南芥中的一些免疫相关防御。在这里，我们建议确定SCP8中免疫抑制活性所需的结构基序。我们进一步建议使用复杂的蛋白质-蛋白质相互作用技术和前向遗传筛选来识别可能与SCP8相互作用的植物蛋白，这些蛋白参与了SCP8介导的免疫抑制。我们的工作旨在从分子上了解质外体真菌效应器如何通过干扰某些但不是所有PRR共享的植物免疫系统成分来操纵植物宿主的免疫激活。这项工作可能证明利用微生物效应器来破译植物免疫信号转导通路的潜力。

Plant innate immunity mediated through membrane-bound pattern recognition receptors (PRRs) is instrumental to protection against microbial infections. However, host-adapted plant pathogenic fungi and oomycetes have evolved apoplastic effectors that manipulate plant extracellular functions in order to establish infection. Recently, we identified a conserved effector protein SCP8 from Verticillium dahliae, a fungal pathogen with a broad host range. SCP8 suppresses some immunity-associated defenses in Arabidopsis mediated through activation of LRR-RK and LRR-RP-type PRRs. Here, we propose to identify structural motifs within SCP8 that are required for its immunosuppressive activity. We further propose to employ sophisticated protein-protein interaction technologies and forward genetic screens to identify putative SCP8-interacting plant proteins involved in SCP8-mediated immune suppression. Our work aims at gaining a molecular understanding of how an apoplastic fungal effector may manipulate plant host immune activation through interference with components of the plant immune system that are shared among certain, but not all PRRs. This work may demonstrate the potential of using microbial effectors to decipher plant immune signal transduction cascades.