Critical Role of Transcription Factor CtSR in Mediating Ergosterol Biosynthesis and DMI Fungicides Sensitivity in Colletotrichum truncatum

Anthracnose caused by Colletotrichum truncatum severely impacts global fruit/vegetable yields. Unlike other Colletotrichum species, C. truncatum exhibits inherent resistance to some sterol demethylation inhibitors (DMIs), necessitating an understanding of ergosterol synthesis regulation and resistance mechanisms. A transcription factor, CtSR (CTRU02_06681), that regulates the DMI sensitivity in C. truncatum was identified in our study. Deletion of CtSR rendered a naturally resistant isolate highly sensitive to DMIs, significantly reduced total ergosterol levels, decreased CYP51s expression compared to the wild type, and abolished DMI-induced expression of CYP51s. Deletion of CtSR reduced mycelial growth and virulence and made the strain highly sensitive to oxidative stress but did not affect its sensitivity to osmotic stress. Transcriptomic analysis and yeast one-hybrid assays confirmed that CtSR directly binds the conserved promoter motif CGAATACGAA to regulate ergosterol biosynthesis genes. Taken together, our study demonstrates a critical role for CtSR in the regulation of ergosterol biosynthesis and DMI interactions in C. truncatum, which may have significant practical implications.