The Mechanism of Fraxetin as a Sustainable Fungicide for Larch Shoot Blight: Lipid Peroxidation and Oxidative Stress in Neofusicoccum laricinum

Larch shoot blight, caused by <i>Neofusicoccum laricinum</i>, threatens global larch resources, while conventional chemical control is constrained by pollution and resistance. To address this gap, we integrated metabolomics, transcriptomics, and antifungal efficacy assays to identify Fraxetin, a disease-induced phytoalexin, and to elucidate its antifungal activity and mechanism. Metabolomics showed infection-triggered accumulation of Fraxetin in resistant <i>Larix olgensis</i> shoots. Antifungal experiments showed that within the range of 68-1088 μg/mL, the optimal antifungal concentration was 1088 μg/mL. When inoculated larches were treated with 1088 μg/mL Fraxetin, the maximum inhibition rate of pathogen growth reached 66.67% within 12 days, and the symptoms of the treated plants were alleviated. Transcriptomics revealed activation of damage responses, disruption of oxidative homeostasis, and compromised membrane integrity in the pathogen under Fraxetin treatment. Physiological measurements confirmed increased lipid peroxidation, redox collapse, membrane leakage, and reduced fungal viability. These findings indicate a lipid peroxidation-mediated oxidative-membrane mode of action and support the potential of plant-derived Fraxetin for more sustainable management of larch shoot blight.