Salicylic acid suppresses ¹O₂-mediated susceptibility to Alternaria alternata in Arabidopsis

Abstract

Necrotrophic Alternaria alternata induces EXECUTER 1(EX1)/2-dependent singlet oxygen (1O2) bursts, leading to plant cell death, with jasmonic acid (JA) acting as a key signal transducer downstream of EX1/2-mediated signaling. Salicylic acid (SA), a crucial defense hormone, is known to respond to pathogen invasion and activate defense gene expression. Previous studies emphasize the importance of SA in A. alternata-induced necrosis in the light of the increased susceptibility of SA-deficient transgenic Arabidopsis NahG to A. alternata. In this study, we investigated the role of SA in A. alternata-triggered 1O2 signaling in Arabidopsis. We found that EX1/2 deficiency did not alter SA levels in Arabidopsis infected with A. alternata, indicating that SA signaling regulates A. alternata-induced pathogenesis through an EX1/2-independent pathway. Exogenous SA application and increased endogenous SA in the ssi2-2 mutant enhanced resistance but inhibited JA production. Conversely, SA signaling deficiency in the eds1 and pad4 mutants increased susceptibility and elevated JA levels. In conclusion, SA enhances Arabidopsis defense against A. alternata via an EX1/2-independent 1O2 signal pathway and antagonizes JA biosynthesis.

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