ArticleBMC microbiology2025
β-caryophyllene regulates H3K36me3 to inhibit conidial germination and mycelial growth of Fusarium proliferatum.
Article in BMC microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- From Nature to Nanotech: Customizing Essential Oil Delivery for a Reduced Fungicide in Agriculture.ACS omega · 2026Review
- Indigenous fungi inoculation drives organic carbon accumulation and phosphorus transformation in coal gangue-based artificial soil: role of mineral-bioactivation.Frontiers in microbiology · 2026Article
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Abstract
backgroundPanax notoginseng is a valuable traditional Chinese medicine and is highly susceptible to root rot disease, which is primarily caused by the pathogenic fungus Fusarium proliferatum. The antifungal mechanisms underlying the effects of β-caryophyllene (BCP), which is commonly found in Essential oils (EOs), remain unclear. In this study, RNA sequencing (RNA-seq) and chromatin immunoprecipitation sequencing (ChIP-seq), along with in vitro antifungal experiments, were used to investigate the inhibitory effects of BCP on F. proliferatum.
resultsBCP not only influenced the mycelial growth of F. proliferatum but also exerted a pronounced inhibitory effect on conidial germination. After treatment with 200 mM BCP, the inhibition rate of mycelial growth was 24.5%, whereas the inhibition rate of conidial germination reached 77.87%. Furthermore, after 4 h of 200 mM BCP treatment, the extracellular conductivity of F. proliferatum significantly increased, along with Malondialdehyde content and superoxide dismutase activity, which increased to 2.6 and 1.45 times those of the control group. Transcriptome analysis revealed that, following BCP treatment, 1693 differentially expressed genes (DEGs) were upregulated and 1589 DEGs were downregulated. Additionally, BCP treatment decreased the expression of genes associated with conidial germination regulation, including the transcriptional activator acu-15, serine/threonine protein phosphatases, and aldehyde dehydrogenases. Combined RNA-seq and ChIP-seq analyses revealed elevated H3K36me3 (histone H3 Lysine 36 trimethylation) modification levels in F. proliferatum after BCP treatment, which triggered defense mechanisms and upregulated the expression of lipid metabolism genes associated with cell membrane repair. Downregulation of the expression of genes associated with decreased H3K36me3 modification in meiosis-related and cell cycle pathways in yeast was observed, which inhibited the expression of serine/threonine protein kinase (SNF1) and the transcription factor MCM1, further suppressing conidial germination and negatively impacting hyphal growth.
conclusionsThis study elucidates the antifungal mechanism of BCP and provides a theoretical foundation for the development of novel plant-derived pesticides for root rot control.
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