Cellular dynamics between PAMP receptors and pathogen-derived effectors

植物主动防御的一个重要方面是检测由细胞表面受体介导的病原相关分子模式（PAMPs）。对于疾病的建立，病原体依赖于克服PAMP感知并使响应于PAMP而激活的植物信号传导途径失效的能力。因此，模式识别受体（PRR）是病原体效应物的主要靶标。FLS 2、其共受体BAK 1和EFR编码受体样激酶（RLK），其在针对细菌病原体的免疫中起作用并负责细菌鞭毛蛋白（flg 22）和EF-Tu（elf 18）的感知，在SPP 1212的第一个资助期内，我们发现番茄致病假单胞菌DC 3000的毒力通过效应子AvrPtoB的作用增强了拟南芥中的PtoDC 3000，这取决于其E3连接酶活性。我们可以证明AvrPtoB与FLS 2的物理关联，其在受体活化后增强。我们可以证明AvrPtoB泛素化FLS 2并促进FLS 2的降解，但不促进BAK 1的降解（Göhre和Spallek等人，修订版）。它仍然保持开放，AvrPtoB使用该植物内途径来实现FLS 2的降解。我们希望确定负责FLS 2泛素化的残基，降解如何与FLS 2激活和运输联系起来，并解决AvrPtoB对PRRs的特异性。看来信号PRR的急性抑制对于病原体毒力很重要，我们建议更多地了解病原体触发的细胞运输重编程。越来越多的效应器被描述为抑制PAMP触发的防御反应，我们想确定那些在PRR水平上起作用的。因为这样的效应物还包括小分子，我们先前鉴定了影响FLS 2内吞作用的化合物并研究了它们在flg 22信号传导中的作用（塞拉诺等人，2007），并且我们想要扩展该研究。BAK 1作为FLS 2的共受体的鉴定（Chinchilla等人，2007 a）显著地推进了我们对受体机制和PAMP信号传导的理解。由于bak 1突变体显示flg 22不敏感，我们确定了几个新的fli（flg 22不敏感）突变体通过遗传筛选。突变体fli 1、fli 3和fli 6在flg 22触发的胼胝质沉积和对细菌感染的抗病性方面受损。在SPP 1212的框架下，我们提出分离fli突变体的责任位点，这些突变体可能是FLS 2运输的调节因子，并且是病原体效应物的潜在靶标。总体而言，我们的研究将为植物免疫受体和病原体模式的相互作用提供新的见解，PAMP被认为是对植物免疫重要的配体，或者被认为是靶向受体以对抗PAMP信号传导的效应物，从而有助于病原体毒力

An important layer of active defense in plant immunity is the detection of pathogenassociated molecular patterns (PAMPs) mediated by cell surface receptors. For the establishment of disease, pathogens depend on the ability to overcome PAMP perception and disable plant signalling pathways activated in response to PAMPs. Pattern recognition receptors (PRRs), therefore, represent prime targets for pathogen effectors. FLS2, its co-receptor BAK1, and EFR encode receptor-like kinases RLKs) that play a role in immunity against bacterial pathogens and are responsible for the perception of bacterial flagellin (flg22) and EF-Tu (elf18), respectively.Within the first funding period of the SPP1212 we discovered that virulence of Pseudomonas syringae pv tomato DC3000 (PtoDC3000) in Arabidopsis was enhanced through the action of the effector AvrPtoB, which was dependent on its E3 ligase activity. We could demonstrate physical association of AvrPtoB with FLS2, which was enhanced upon receptor activation. We could show that AvrPtoB ubiquitinates FLS2 and promotes degradation of FLS2 but not BAK1 (Göhre and Spallek et al, in revision). Still it remains open, which in planta pathway is used by AvrPtoB to achieve degradation of FLS2. We would like to identify the responsible residues for FLS2 ubiquitination, how degradation is connected with FLS2 activation and trafficking and address AvrPtoB specificity to PRRs. It appears that acute inhibition of signalling PRRs is important for pathogen virulence, which we propose to gain more insights into pathogen-triggered reprogramming of cellular trafficking. An increasing number of effectors are described to suppress PAMPtriggered defense responses and we would like to identify those acting at the level of PRRs. Because such effectors include also small molecules, we previously identified compounds that affect FLS2 endocytosis and investigated their role in flg22 signalling (Serrano et al, 2007), and we would like to extend this study.The identification of BAK1 as co-receptor of FLS2 (Chinchilla et al, 2007a) significantly advanced our understanding of receptor mechanisms and PAMP signalling. Since bak1 mutants display insensitivity to flg22, we identified several novel fli (flg22-insensitive) mutants through a genetic screen. The mutants fli1, fli3, and fli6 are impaired in flg22- triggered callose deposition and disease resistance to bacterial infection. In the frame of the SPP1212 we propose to isolate the responsible loci of fli mutants, which could be regulators of FLS2 trafficking and are potential targets of pathogen effectors.Overall, our studies should provide novel insights into the interaction of plant immune receptors and pathogen patterns, either PAMPs perceived as ligands important for plant immunity or as effectors that target the receptors to counter act PAMP signalling and thereby contribute to pathogen virulence.