Cyril Zipfel

Welcome

Higher eukaryotes can recognize invading microorganisms by detecting conserved molecules referred to as PAMPs (pathogen-associated molecular patterns) by pattern recognition receptors (PRRs). The mechanisms underlying this innate immune recognition and subsequent signalling have been extensively studied over the last decade in insects and mammals, but much remains to be discovered in plants. 

Arabidopsis thaliana provides an excellent model system to study PAMP-triggered immunity (PTI), and detects a variety of PAMPs including conserved domains of bacterial flagellin and EF-Tu, or their peptide surrogates, flg22 and elf18, respectively. The related LRR receptor kinases (LRR-RLKs) FLS2 and EFR are the PRRs for flagellin and EF-Tu, respectively. They are so far the only known Arabidopsis PRRs, and also the only known plant PRRs that recognize bacterial PAMPs. FLS2 and EFR trigger a MAP kinase cascade, rapid induction of many defence-related genes, increases in reactive oxygen species (ROS) and ethylene production, callose deposition, and seedling growth inhibition.

The significance of PAMP-triggered immunity (PTI) against bacteria is demonstrated by the fact that successful bacterial pathogens have evolved to avoid PAMP recognition or to suppress PTI-signalling by secreting effectors into the host cells. Importantly, both fls2 and efr mutant plants are more susceptible to bacterial infections. Although many resistance (R) proteins have been identified and many genetic or biochemical approaches to dissecting effector-triggered immunity (ETI) initiated, there is only limited knowledge about plant PRRs and PRR signal transduction.

Many phenomena have been correlated with flg22 responses, but the order of events and the mechanisms required have not been subjected to genetic analysis. We need to understand PTI properly not only because of its intrinsic interest, but because many of the pathogen effector targets will be PTI components. Furthermore, there are more PRRs to discover in order to fully understand the molecular interplay between host and pathogen that directs the outcome of infection.  We are using a combination of forward- and reverse-genetics, as well as biochemical and proteomic approaches to answer the main questions underlying our research program:

  • How are PAMP perceived?
  • What are the signalling events downstream of PAMP perception?
  • What is the contribution of PAMP perception to plant immunity?