Fig. 3: Impairing the Erg11-Ncp1 interaction enhances the susceptibility of C. albicans to azoles.

a The schematic diagram illustrating the generation of the erg11^m/erg11Δ mutant involved the insertion of synthesized Erg11^m at the ADE2 gene locus in the heterozygous deleted mutant ERG11/erg11Δ. Subsequently, the ARG4 gene was employed to replace the remaining allele of the ERG11 gene, resulting in the creation of the erg11^m/erg11Δ mutant, where Erg11^m and Ncp1 were found to be incapable of interacting. b Spotting assays were conducted to assess the hypersensitivity of the erg11^m/erg11Δ mutant to fluconazole (FLC) in comparison to the wild-type strain SN152 and the ERG11/erg11Δ, NCP1/ncp1Δ, erg11Δ/erg11Δ, and ncp1Δ/ncp1Δ mutants on YPD plates with or without 4 μg/mL FLC. Images of the cultured cells were captured after 48 h of incubation at 30 °C. c The FLC disk diffusion assays were conducted on the erg11^m/erg11Δ mutant, which exhibited a larger and cleaner inhibition zone on plates compared to the wild-type strain SN152 and the mutants of ERG11/erg11Δ, NCP1/ncp1Δ, erg11Δ/erg11Δ, and ncp1Δ/ncp1Δ. d The MIC assays were conducted to evaluate the hypersensitivity of the erg11^m/erg11Δ mutant to FLC contrasted with the wild-type strain SN152 and the mutants of ERG11/erg11Δ, NCP1/ncp1Δ, erg11Δ/erg11Δ, and ncp1Δ/ncp1Δ. “NA” stands for “not applicable”. e The MIC assays demonstrated that ergosterol was ineffective in completely mitigating the antifungal effects of FLC in the erg11^m/erg11Δ mutant. “NA” stands for “not applicable”. Source data are provided as a Source Data file.