Poster
Ye Jin Ahn
Seoul National University
Seoul, South Korea, KOREA
Haseong Kim
University of Tubingen
Tubingen, Baden-Wurttemberg, Germany
Alex Schultink
CEO
Fortiphyte
Richmond, California, United States
Kee Hoon Sohn, PhD (he/him/his)
Associate Professor
Seoul National University
Seoul, Seoul-t'ukpyolsi, Republic of Korea
The coevolution of plants and pathogens drives the dynamic evolution of plant immune systems. Pathogen effectors target various host proteins for pathogen survival in the host. As one of the strategies for effector recognition, plants have evolved decoys, host target proteins that signal nucleotide-binding leucine-rich repeat receptors (NLRs) to activate immunity. One of the most well-known decoys in Arabidopsis is RPM1-INTERACTING PROTEIN 4 (RIN4), and AvrRpt2, AvrRpm1, AvrB, and HopZ5 from Pseudomonas, as well as AvrBsT from Xanthomonas, have been shown to modify RIN4 post-translationally and activate immunity. In distantly related Nicotiana benthamiana, Pseudomonas tomato race 1 (NbPtr1) can recognize all five effectors. To understand the mechanism of expanded effector recognition of NbPtr1, we investigated RIN4 homologs and proteins that carry nitrate-induced domains (NOI), which are key functional domains of RIN4. We discovered that five N. benthamiana NOI proteins (NbNOIs), not RIN4 homologs, could suppress programmed cell death induced by the overexpression of NbPtr1. Silencing the five NbNOIs through virus-induced gene silencing resulted in a lethal phenotype dependent on NbPtr1 activity. These results suggest that NbNOIs negatively regulate NbPtr1 and function as decoys. Understanding the function of the diversified family of NbNOIs will help understand the mechanism behind the expanded effector recognition of NLRs.