A receptor-like protein from Nicotiana benthamiana mediates VmE02 PAMP-triggered immunity.

Plants use their innate immune system to defend against phytopathogens. As a part of this, pattern triggered-immunity is activated via pattern recognition receptor (PRR) detection of pathogen-associated molecular patterns (PAMPs). Although an increasing number of PAMPs have been identified, the PRRs for their recognition remain largely unknown. In the present study, we report a receptor-like protein RE02 (Response to VmE02) in Nicotiana benthamiana, which mediates the perception of VmE02, a PAMP previously identified from the phytopathogenic fungus Valsa mali, using virus-induced gene silencing (VIGS), co-immunoprecipitation, pull-down and microscale thermophoresis assays. We show that silencing of RE02 markedly attenuated VmE02-triggred cell death and immune responses. RE02 specifically interacted with VmE02 in vivo and in vitro, and it displayed a high affinity for VmE02. Formation of a complex with the receptor-like kinases SOBIR1 and BAK1 was essential for RE02 to perceive VmE02. Moreover, RE02-silenced plants exhibited enhanced susceptibility to both the oomycete Phytophthora capsici and the fungus Sclerotinia sclerotiorum, while overexpression of RE02 increased plant resistance to these pathogens. Together, our results indicate that the PAMP VmE02 and the receptor-like protein RE02 represent a new ligand-receptor pair in plant immunity, and that RE02 represents a promising target for engineering disease resistance.