Plant-derived citronellol can significantly disrupt cell wall integrity maintenance of Colletotrichum camelliae.

Anthracnose, a fungal disease, commonly infects tea plants and severely impacts the yield and quality of tea. One method for controlling anthracnose is the application of citronellol, a plant extract that exhibits broad-spectrum antimicrobial activity. Herein, the physiological and biochemical mechanism by which citronellol controls anthracnose caused by Colletotrichum camelliae was investigated. Citronellol exhibited excellent antifungal activity based on direct and indirect mycelial growth inhibition assays, with EC 50 values of 76.88 mg/L and 29.79 μL/L air, respectively. Citronellol also exhibited good control effects on C. camelliae in semi-isolated leaf experiments. Optical and scanning electron microscopy revealed that citronellol caused C. camelliae mycelia to thin, fracture, fold and deform. Transmission electron microscopy revealed that the mycelial cell walls collapsed inward and separated, and the organelles became blurred after treatment with citronellol. The sensitivity of C. camelliae to calcofluor white staining was significantly enhanced by citronellol, while PI staining showed minimal fluorescence, and the relative conductivity of mycelia were not significantly different. Under citronellol treatment, the expression levels of β -1,3-glucanase, chitin synthase, and chitin deacetylase-related genes were significantly decreased, while the expression levels of chitinase genes were increased, leading to lower chitinase activity and increased β -1,3-glucanase activity. Therefore, citronellol disrupted the cell wall integrity of C. camelliae and inhibited normal mycelial growth. [Display omitted] • Citronellol significantly exhibited the growth of Colletotrichum camelliae based on direct and indirect mycelial growth inhibition assays. • Citronellol could disrupt cell walls integrity, thereby inhibiting the mycelial growth of C. camelliae. • Citronellol might enhance the expression levels of β -1,3-glucanase-related genes, thereby increasing β -1,3-glucanase activity and promoting the degradation of cell wall components β -1,3-glucan. [ABSTRACT FROM AUTHOR]