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

Jinlong Zhang,Lili Huang,Mingxia Zhou,Jiajun Nie,Wei Liu

doi:10.3390/ijms23010508

Abstract

Kiwifruit canker, caused by Pseudomonas syringae pv. actinidiae (Psa), 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 Psa and their function mechanism remain largely unclear. Here, we successfully identified a T3SS effector HopAU1 which had no virulence contribution to Psa, but could, however, induce cell death and activate a series of immune responses by agroinfiltration in Nicotiana benthamiana, 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 N. benthamiana (NbCaS) as well as its close homologue in kiwifruit (AcCaS). More importantly, silencing CaS by RNAi in N. benthamiana greatly attenuated HopAU1-triggered cell death, suggesting CaS is a crucial component for HopAU1 detection. Further researches showed that overexpression of NbCaS in N. benthamiana significantly enhanced plant resistance against Sclerotinia sclerotiorum and Phytophthora capsici, indicating that CaS 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.

Highlights

Central to plant survival is the ability to activate immunity upon pathogen perception.Plant immunity is activated by sensing either conserved microbial signatures like pathogenassociated molecular patterns (PAMPs) or specific effectors secreted by pathogens [1]
To test whether HopAU1induced cell death had a relationship with plant immunity response, we examined the accumulation of reactive oxygen species (ROS) burst and callose deposition, and the transcript accumulation levels of two corresponding signal pathway marker genes, HSR203J
To test whether HopAU1induced cell death had a relationship with plant immunity response, we examined the accumulation of reactive oxygen species (ROS) burst and callose deposition, and the transcript accumulation levels of two corresponding signal pathway marker genes, HSR203J and HIN1 [34,35], in N. benthamiana

Summary

Introduction

Central to plant survival is the ability to activate immunity upon pathogen perception. Plant immunity is activated by sensing either conserved microbial signatures like pathogenassociated molecular patterns (PAMPs) or specific effectors secreted by pathogens [1]. Effector-triggered immunity (ETI) through intracellular receptors interferes with pathogen invasion early in host and converts it to rapid and robust defense [2]. During the course of their co-evolution, it increases the challenge of resistance breeding for preventing disease. Resistance breeding has been demonstrated to be one of the most efficient strategies for disease management. For disease-resistance breeding, the application of resistancerelated genes is dramatically timesaving, compared with the conventional hybrids breeding approach [3]. It remains a big challenge to obtain resistance-related genes before their successful application into breeding

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