Neofusicoccum laricinum is the causal agent of larch shoot blight, a fungal disease affecting several species of larch. It causes severe damage, including stunting and mortality. This study aims to address the severe impact of larch shoot blight by evaluating the effect of farrerol on the inhibition of Neofusicoccum laricinum in Larix olgensis. We used LC-MS/MS and weighted gene co-expression network analysis to investigate farrerol’s effects on Neofusicoccum laricinum and identify associated genes in resistant and susceptible larch. Our study identified significant differences in metabolite profiles between resistant and susceptible cultivars, with higher concentrations of farrerol showing complete inhibition of N. laricinum. Additionally, specific genes associated with farrerol content were up-regulated in resistant larch. Farrerol at higher concentrations completely inhibited N. laricinum, showing a strong correlation with increased disease resistance. This research suggests that farrerol enhances disease resistance in larch and provides a foundation for developing disease-resistant larch varieties based on antifungal metabolite traits.

Neofusicoccum laricinum, the pathogen responsible for larch shoot blight, is a hemibiotrophic pathogen. A hypersensitive reaction of plants does not inhibit the growth of the pathogen, while phytoalexin is an antifungal compound secreted by plants, which can directly destroy the cells of pathogens and help plants achieve resistance. This study aimed to investigate the chemical defense mechanisms in resistant larch, identify key biocontrol agents, and assess their potential for field application. By integrating multi-omics technologies with time-dependent models and dose–response curve analysis, the accumulation and antimicrobial properties of rutaevin were examined. Its application potential was verified through cross-species resource screening and field trials. The results revealed that rutaevin acts as a phytoalexin against larch shoot blight. It began to accumulate linearly 0.62 days after pathogen exposure, with its antifungal activity demonstrating a dose-dependent response, achieving 100% inhibition at 0.5 mg/mL. The activation of terpene metabolic pathways in disease-resistant plants resulted in a significant increase in rutaevin content compared to susceptible plants. Cross-species screening showed that the highest concentration of this compound is found in the fruit of Evodia rutaecarpa var. rutaecarpa, with its crude extract exhibiting strong field efficacy. The findings provide theoretical and technical support for disease-resistant breeding and the development of plant-derived fungicides.

Larch shoot blight, caused by Neofusicoccum laricinum, 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 Larix olgensis 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.

Pine wood nematodes (Bursaphelenchus xylophilus, PWNs) are a major threat to Pinus koraiensis in northeast China, and emamectin benzoate (EB) is commonly used for their control. Although high doses of EB can alleviate symptoms of pine wilt disease (PWD), they do not fully eradicate PWNs due to their detoxification mechanisms. This study investigates the content of EB in P. koraiensis and its efficacy in controlling PWNs after exogenous application of EB. We found that while EB significantly reduced PWN populations, it did not eliminate them. Transcriptomic analysis of PWNs treated with concentration at 20% (LC₂₀) revealed that PWNs exhibit detoxification responses to low EB concentrations (LC₂₀), driven by the Bx-SDR3 gene. RNA interference (RNAi)-mediated silencing of this gene decreased the detoxification ability of PWNs and enhanced the toxic effects of LC₂₀ EB by 20.9%. These results highlight the key role of Bx-SDR3 in PWN detoxification and suggest that targeting this gene could improve the effectiveness of EB, offering a promising strategy for more efficient and eco-friendly pest management.