The Phytophthora sojae RXLR effector Avh238 destabilizes soybean Type2 GmACSs to suppress ethylene biosynthesis and promote infection.

Abstract

Phytophthora pathogens secrete many effector proteins to manipulate host innate immunity. PsAvh238 is a Phytophthora sojae N-terminal Arg-X-Leu-Arg (RXLR) effector, which evolved to escape host recognition by mutating one nucleotide while retaining plant immunity-suppressing activity to enhance infection. However, the molecular basis of the PsAvh238 virulence function remains largely enigmatic. By using coimmunoprecipitation and liquid chromatography-tandem mass spectrometry analysis, we identified the 1-aminocyclopropane-1-carboxylate synthase (ACS) isoforms, the key enzymes in ethylene (ET) biosynthesis, as a host target of PsAvh238. We show that PsAvh238 interacts with soybean ACSs (GmACSs) in\xa0vivo and in\xa0vitro. By destabilizing Type2 GmACSs, PsAvh238 suppresses Type2 ACS-catalyzed ET biosynthesis and facilitates Phytophthora infection. Silencing of Type2 GmACSs, and inhibition of ET biosynthesis or signaling, increase soybean susceptibility to P.\xa0sojae infection, supporting a role for Type2 GmACSs and ET in plant immunity against P.\xa0sojae. Moreover, wild-type P.\xa0sojae but not the PsAvh238-disrupted mutants, inhibits ET induction and promotes P.\xa0sojae infection in soybean. Our results highlight the ET biosynthesis pathway as an essential part in plant immunity against P.\xa0sojae and a direct effector target.