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Comparative Analysis of Signaling Pathways Triggered by Different Pattern-recognition Receptor-types

by WanWei-Lin

Institution: Universitt Tbingen
Year: 2017
Posted: 02/01/2018
Record ID: 2151410
Full text PDF: http://hdl.handle.net/10900/79168


Abstract

Plant cell surface receptors sense microbial pathogens by recognizing microbial structures called pathogen or microbe-associated molecular patterns (PAMPs/MAMPs). There are two major types of plant pattern recognition receptors: 1. Leucine-rich repeat receptor proteins (LRR-RP) and LRR receptor kinases (LRR-RK) and 2. Plant receptor proteins and receptor kinases carrying ectopic lysin motifs (LysM-RP and LysM-RK). Although many studies focused on the signal pathways triggered by these receptors individually, the exact overlap and the differences, respectively, between these pathways remain largely unknown. In this study, Arabidopsis thaliana responses to three different MAMPs, flg22, nlp20, chitin (C6), via their corresponding receptor types, FLS2 (LRR-RK), RLP23 (LRR-RP), CERK1 (LysM-RK) were compared. Systematic analyses of various plant immune responses revealed that nlp20 triggers only slow and weak early responses such as ROS accumulation and MAPK activation. However, compared to flg22, nlp20 is capable of inducing higher levels of the phytohormones ethylene and salicylic acid. In contrast, flg22 triggers early responses (ROS, MAPKs) faster and stronger, and also causes more extensive transcriptome reprogramming. Both flg22 and nlp20 cause callose deposition, but only treatment with nlp20 results in the accumulation of the phytohormone camalexin. Additionally, the LysM-RK-ligand C6 can trigger strong early responses, but fails to induce late responses. The two peptides nlp20 and flg22 are recognized by the LRR-RP RLP23 (together with its adaptor kinase SOBIR1) and the LRR-RK FLS2, respectively, and both receptor complexes recruit the co-receptor LRR-RLK BAK1 after ligand perception. However, whereas BAK1 is indispensable for FLS2 function, it can be partially replaced by other BAK1 family members in RLP23-mediated nlp20 signaling. Analysis of further mutant lines indicated that the regulatory proteins BIR2, CPK28, PP2A, and G proteins impinge on both flg22- and nlp20-triggered signaling in a similar way. Surprisingly, BIK1, which is a positive regulator in flg22-triggered signaling pathway, was shown here to negatively regulate nlp20-induced immune responses. Thus, higher levels of ROS, ethylene, SA and camalexin were measured in the bik1 and bik1 pbl1 mutants after nlp20 treatment than in the wild type control. However, the molecular mechanism of how BIK1 differently regulates flg22- and nlp20-triggered signaling pathways still remains to be clarified.Advisors/Committee Members: Nrnberger, Thorsten (Prof. Dr.) (advisor).

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