Identification of signaling components leading to induction of plant defense responses mediated by the MAMP EIX
A. AVNI (1) (1) Tel Aviv University, Israel

The activation of defense responses is mediated by the specific recognition of the invading pathogen. These defense mechanisms are triggered by pathogen-derived molecules defined as elicitors; microbial associated molecular pattern (MAMP). LeEix2 acts as a functional receptor for the MAMP EIX. Furthermore, the binding of EIX to LeEix2 protein induces receptor-mediated endocytosis, thus allowing the receptor to initiate, through interacting proteins, a signal transduction cascade leading to the induction of defense responses. In order to identify and characterize proteins involved in the LeEIX2-EIX mediated defense response, split-ubiquitin yeast two-hybrid (Y2H) screenings were conducted, using LeEix2 receptor as bait. The screens revealed several potential interactors. One of the identified interactors was homologous to a receptor-like protein kinase (RLK) from Arabidopsis (At5g24010), and was chosen for further analysis (termed SlRLK-like). SlRLK-like is highly similar to the extracellular domain of the At5g24010 gene of Arabidopsis thaliana. At5g24010 belongs to the CrRLK family (Catharanthus roseus protein-kinase-1-like), which has in vitro characterized kinase activity. The interaction between LeEix2 and the above RLK was re-confirmed using bimolecular fluorescence complementation (BiFC) and co-immunopurification (CoIP) assays. These experiments indicated that the proteins interact in planta and that the interaction is effected by EIX elicitation. Over-expression of the above SlRLK-like negatively affects various EIX-mediated defense responses, such as ethylene biosynthesis, ROS production and HR development. SlRLK-like also interacted with the RLK FLS2, as was observed in CoIP, and its over-expression reduced flg22-mediated ROS production. Our results suggest that SlRLK-like may act as a negative regulator of defense response initiated both by RLPs and RLKs

Abstract Number: P17-489
Session Type: Poster