Pseudomonas syringae pv. actinidiae Effector HopAU1 Interacts with Calcium-Sensing Receptor to Activate Plant Immunity

Abstract

Kiwifruit canker, caused by <i>Pseudomonas syringae</i> pv. <i>actinidiae</i> (<i>Psa</i>), is a destructive pathogen that globally threatens the kiwifruit industry. Understanding the molecular mechanism of plant-pathogen interaction can accelerate applying resistance breeding and controlling plant diseases. All known effectors secreted by pathogens play an important role in plant-pathogen interaction. However, the effectors in <i>Psa</i> and their function mechanism remain largely unclear. Here, we successfully identified a T3SS effector HopAU1 which had no virulence contribution to <i>Psa</i>, but could, however, induce cell death and activate a series of immune responses by agroinfiltration in <i>Nicotiana benthamiana</i>, including elevated transcripts of immune-related genes, accumulation of reactive oxygen species (ROS), and callose deposition. We found that HopAU1 interacted with a calcium sensing receptor in <i>N. benthamiana</i> (NbCaS) as well as its close homologue in kiwifruit (AcCaS). More importantly, silencing <i>CaS</i> by RNAi in <i>N. benthamiana</i> greatly attenuated HopAU1-triggered cell death, suggesting CaS is a crucial component for HopAU1 detection. Further researches showed that overexpression of <i>NbCaS</i> in <i>N. benthamiana</i> significantly enhanced plant resistance against <i>Sclerotinia sclerotiorum</i> and <i>Phytophthora capsici</i>, indicating that <i>CaS</i> serves as a promising resistance-related gene for disease resistance breeding. We concluded that HopAU1 is an immune elicitor that targets CaS to trigger plant immunity.