The Zygotic Division Regulator ZAR1 Plays a Negative Role in Defense Against Botrytis cinerea in Arabidopsis

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.

Automated summary

The phosphorylation/dephosphorylation cycle at tyrosine 428 of CHITIN ELICITOR RECEPTOR KINASE 1 (CERK1) is essential for chitin triggered immunity in Arabidopsis thaliana. ZYGTIC ARREST 1 (ZAR1) interacts with CERK1 specifically when the tyrosine 428 residue of CERK1 is dephosphorylated. ZAR1, originally known for its role in regulating zygotic division, also negatively contributes to defense against Botrytis cinerea and has a redundant role with its homolog ZAR2 in this process.