Abstract

A phosphorylation/dephosphorylation cycle at tyrosine 428 of CHITIN ELICITOR RECEPTOR KINASE 1 (CERK1) plays an essential role in chitin triggered immunity in Arabidopsis thaliana. In this study, we used a differential peptide pull-down (PPD) assay to identify factors that could participate downstream of this cycle. We identified ZYGOTIC ARREST 1 (ZAR1) and showed that it interacts with CERK1 specifically when the tyrosine 428 (Y428) residue of CERK1 is dephosphorylated. ZAR1 was originally characterized as an integrator for calmodulin and G-protein signals to regulate zygotic division in Arabidopsis. Our current results established that ZAR1 also negatively contributed to defense against the fungus Botrytis cinerea and played a redundant role with its homolog ZAR2 in this process. The zar1-3 zar2-1 double mutant exhibited stronger resistance to B. cinerea compared with zar1-3 single mutant, zar2-1 single mutant, and wild-type plants. Moreover, the inducible expression of numerous defense response genes upon B. cinerea infection was increased in the zar1-3zar2-1 double mutant, consistent with a repressive role for ZAR proteins in the defense response. Therefore, our findings provided insight into the function of ZAR1 in multiple defenses and developmental regulation pathways.

Highlights

  • Plants confront attacks from various pathogens and have developed immunity mechanisms to defend against pathogen infection

  • We reported that the leucine-rich repeat receptor-like kinase (RLK) (LRR-RLK) ZYGOTIC ARREST 1 (ZAR1) could interact with CHITIN ELICITOR RECEPTOR KINASE 1 (CERK1) when it harbored the dephosphorylated Y428 residue and that ZAR1 negatively contributed to the defense against Botrytis cinerea in Arabidopsis

  • Plants have evolved various cell-surface RLKs that perceive diverse signals, such as phytohormones and peptides derived from plants, and pattern molecules derived from microbes

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Summary

INTRODUCTION

Plants confront attacks from various pathogens and have developed immunity mechanisms to defend against pathogen infection. In Arabidopsis, the chitin elicitor receptor kinase 1 (CERK1)/LysM-RLK1 is an indispensable receptor-like kinase (RLK) for chitin-triggered immunity signaling (Miya et al, 2007; Wan et al, 2008; Liu et al, 2012). Both heterodimerization between CERK1 and LYK5 and chitintriggered homodimerization of CERK1 play essential roles in chitin signaling in Arabidopsis (Liu et al, 2012; Cao et al, 2014). We reported that the leucine-rich repeat RLK (LRR-RLK) ZYGOTIC ARREST 1 (ZAR1) could interact with CERK1 when it harbored the dephosphorylated Y428 residue and that ZAR1 negatively contributed to the defense against Botrytis cinerea in Arabidopsis

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