Abstract

Fusarium oxysporum disrupts redox homeostasis in Vigna mungo, likely by interfering with salicylic acid signaling, which can be ameliorated by boosting PAL and its related pathways via salicylic acid pretreatment. Fusarium oxysporum, a widespread soil-borne fungus, significantly threatens global crops. This study centers on elucidating the infection strategies employed by F. oxysporum against a new and underexplored host Vigna mungo, a leguminous crop of high agronomic value, and the defense mechanisms that can be activated against the infection, aiming to uncover how these responses can be leveraged to develop potential countermeasures. Building on prior work demonstrating the in vitro antifungal efficacy of phytohormones, including salicylic acid (SA), this study further investigates SA pretreatment at 100µM, which previously reduced reactive oxygen species (ROS) and improved germination under Fusarium stress. Through a comprehensive analysis of V. mungo plants pretreated with SA and subjected to F. oxysporum infection, we observed that fungal exposure reduced growth, chlorophyll content, and levels of proteins, phenolics and flavonoids, while increasing stress markers and antioxidant activity. SA pretreatment mitigated these effects by boosting antioxidant molecules and activating the phenylalanine ammonia-lyase (PAL) pathway, thereby enhancing endogenous SA and ROS scavenging. Furthermore, qRT-PCR analysis confirmed SA-mediated upregulation of antioxidant (catalase and peroxidase), fungal stress response genes ((pathogenesis-related gene 4 (PR4) and defensin (DEF)) and SA synthesis and regulator genes (PAL and WRKY70) involved in plant systemic resistance, while LC-MS data revealed an altered metabolic profile with increased phytoalexins and antioxidants synthesis. Overall, SA pretreatment confers resistance against F. oxysporum in V. mungo by modulating endogenous SA and metabolic profile to activate key defense pathways and redox homeostasis, highlighting its potential in plant defense strategies and reinforcing our proposed model of SA action.

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