MOB proteins as novel regulators of pathogen-associated molecular pattern-triggered immunity in Arabidopsis thaliana

• Applicant: Professor Dr. Martin Stegmann
• Subject Area: Plant Biochemistry and Biophysics ; Plant Genetics and Genomics
• Term: from 2014 to 2018
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 271734448

Plants, like animals, utilize surface-localized receptors to sense microbial proteins in the apoplast and trigger an early immune response known as pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI). Archetypal examples of such receptors are the receptor kinases FLS2 and EFR, which bind the bacterial PAMPs flagellin and elongation factor-Tu, respectively. Immunity mediated by FLS2 and EFR depends on the co-receptor BAK1 that heteromerizes with the main receptors immediately following ligand binding. Despite recent advances, the signalling events that occur downstream of receptor activation remain elusive. The proposed research takes advantage of unique tools available in the host laboratory to uncover the genetic mechanisms underlying PTI using mutants recently identified in a novel forward-genetic screen in the model plant Arabidopsis thaliana. This screen utilized the novel mutant bak1-5, which is specifically impaired in PTI but does not exhibit other pleiotropic phenotypes normally observed in bak1 null mutants. This proposal aims at characterizing modifier of bak1-5 (mob) mutants and corresponding proteins. The mob mutants restore PAMP-triggered responses in the bak1-5 mutant background, including immunity to bacteria. Preliminary data suggest that one mutant affects the subtilisin-like serine protease S1P, which was previously shown to process propeptides in different biological pathways. An important example is the cleavage of the pro-peptide leading to the release of the RALF23 peptide. Notably, bioinformatics analysis in the host lab identified the gene encoding RALF23 as a key hub in an flg22-dependent gene expression network and therefore indicating a function of this peptide in PTI signalling. RALF23 belongs to a 3-member gene cluster including RALF33 and the root-specific RALF1. Interestingly, RALF1 was recently shown to be perceived by the RK FERONIA (FER) and, notably, fer mutants show an increased flg22-triggered ROS burst and enhanced disease resistance to Pseudomonas syringae infections. Therefore, our working model is that S1P cleaves PRORALF23 and/or PRORALF33 to release the active peptide, which in turn binds to FER (or a related protein) resulting in the inhibition of PTI signalling, suggesting a previously unknown mechanism for the regulation of PTI. The main goal of this research proposal is to challenge this novel and exciting hypothesis.

• DFG Programme: Research Fellowships
• International Connection: United Kingdom
• Host: Professor Dr. Cyril Zipfel