Peronophythora litchii RXLR effector PlAvh202 destabilizes a host ethylene biosynthesis enzyme.

Oomycete pathogens can secrete hundreds of effectors into plant cells to interfere with the plant immune system during infection. Here, we identified a RXLR effector protein from the most destructive pathogen of litchi (Litchi chinensis Sonn.), Peronophythora litchii, and named it Peronophythora litchii Avirulence homolog 202 (PlAvh202). PlAvh202 could suppress cell death triggered by Infestin 1 (INF1) or Avirulence protein 3a/Receptor protein 3a (Avr3a/R3a) 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 LcSAMS and ET positively regulate litchi immunity towards P. litchii. Overall, these findings highlight that SAMS can be targeted by the oomycete RXLR effector to manipulate ET-mediated plant immunity.