Sterol 14α-Demethylase CaCYP51A and CaCYP51B are Functionally Redundant, but Differentially Regulated in Colletotrichum acutatum: Responsibility for DMI-Fungicide Resistance

Colletotrichum acutatum, the main pathogen causing anthracnose on chili worldwide, is controlled by tebuconazole [a sterol C14-demethylation inhibitor (DMI) fungicide, abbreviated as Teb] with excellent efficacy. Our previous study exhibited that all C. acutatum isolates were sensitive to Teb while the Colletotrichum gloeosporioides population had developed resistance to Teb on the same fungicide-pressure selection. Therefore, the assessment of Teb-resistance in C. acutatum is impending. Twenty Tebresistant (Teb) mutants obtained by fungicide domestication and ultraviolet (UV)-mutagenesis displayed similar fitness compared to parental isolates. Data in the current study exhibited that mutations at CaCYP51A and/or overexpression of CaCYP51s were responsible for Teb-resistance. Furthermore, the deletion mutants Delta CaCYP51A and Delta CaCYP51B played different roles in sensitivities to DMIs. Taken together, this study first reported that mutations at CaCYP51A and/or overexpression of CaCYP51s conferred resistance to Teb in C. acutatum, CaCYP51A and CaCYP51B are functionally redundant, but differentially regulated in DMI resistance.

Automated summary

This study first reported that mutations at CaCYP51A and/or overexpression of CaCYP51s conferred resistance to Teb in C. acutatum. CaCYP51A and CaCYP51B are functionally redundant but differentially regulated in DMI resistance.