Related Experiment Video
Updated: Jul 29, 2025

Functional Characterization of RING-Type E3 Ubiquitin Ligases In Vitro and In Planta
Published on: December 5, 2019
Peronophythora litchii RXLR effector P. litchii avirulence homolog 202 destabilizes a host ethylene biosynthesis
Peng Li1, Wen Li1, Xiaofan Zhou2
1Guangdong Key Laboratory of Microbial Signals and Disease Control/Department of Plant Pathology, College of Plant Protection, South China Agricultural University, Guangzhou 510642, China.
Abstract:
Oomycete pathogens can secrete hundreds of effectors into plant cells to interfere with the plant immune system during infection. Here, we identified a Arg-X-Leu-Arg (RXLR) effector protein from the most destructive pathogen of litchi (Litchi chinensis Sonn.), Peronophythora litchii, and named it P. litchii avirulence homolog 202 (PlAvh202). PlAvh202 could suppress cell death triggered by infestin 1 or avirulence protein 3a/resistance protein 3a in Nicotiana benthamiana and was essential for P. litchii virulence. In addition, PlAvh202 suppressed plant immune responses and promoted the susceptibility of N. benthamiana to Phytophthora capsici. Further research revealed that PlAvh202 could suppress ethylene (ET) production by targeting and destabilizing plant S-adenosyl-L-methionine synthetase (SAMS), a key enzyme in the ET biosynthesis pathway, in a 26S proteasome-dependent manner without affecting its expression. Transient expression of LcSAMS3 induced ET production and enhanced plant resistance, whereas inhibition of ET biosynthesis promoted P. litchii infection, supporting that litchi SAMS (LcSAMS) and ET positively regulate litchi immunity toward P. litchii. Overall, these findings highlight that SAMS can be targeted by the oomycete RXLR effector to manipulate ET-mediated plant immunity.
Related Concept Videos
Cell Signaling in Plants
Stringent Response in E. coli
Defenses Against Pathogens and Herbivores

