Scopoletin negatively regulates the HOG pathway and exerts antifungal activity against Botrytis cinerea by interfering with infection structures, cell wall, and cell membrane formation

Abstract

AbstractBotrytis cinerea is the causative agent of gray mold, a fungal disease affecting a broad array of food crops and resulting in considerable agricultural and economic losses. Currently, chemical fungicides are the most effective control measure, but this practice is challenged by the growing resistance of pathogens to these fungicides. Scopoletin, a major phytoalexin of tobacco plants, has shown promise as an antifungal treatment. Here, we found that scopoletin was effective against B. cinerea infection of tomato leaves. It inhibited mycelial growth and conidial germination of B. cinerea and disrupted cell wall, cell membrane, and infection structure formation. Transcriptomic analysis identified 3495 differentially expressed genes in response to scopoletin treatment. Interestingly, scopoletin seems to deactivate the HOG pathway of B. cinerea. The growth defect caused by hyperactivation of the pathway, such as iprodione treatment and deletion of BcPtc1, the negative regulator of this pathway, was partly rescued by scopoletin. Moreover, it could downregulate phosphorylation levels of BcSak1 treated with iprodione and NaCl. In addition, the control efficiency of triadimefon was significantly increased by scopoletin. Thus, scopoletin is a promising, naturally derived, and sustainable treatment for gray mold, especially when combined with triadimefon.