Cellular dynamics between PAMP receptors and pathogen-derived effectors

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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.