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Peer-reviewedCC BY 4.0International Journal of Molecular Sciences

Sfp1 Contributes to Fluconazole Responses and Virulence in Candida albicans

  • Wei-Luen Huang1
  • Hsuan-Yu Chen1
  • Kuo-Yun Tseng2
  • Dinh-Dong Le1
  • Shin-Huey Lin3
  • Yu-Shan Chang4
  • I-Ching Wang3
  • Hsiu-Jung Lo2,5
  • Chi-Jan Lin4
  • Chung-Yu Lan1,6,7
7 affiliations
  1. 1Institute of Molecular and Cellular Biology, National Tsing Hua University, Hsinchu 300044, Taiwan
  2. 2Taiwan Mycology Reference Center, National Institute of Infectious Diseases and Vaccinology, National Health Research Institutes, Miaoli County 350401, Taiwan
  3. 3Institute of Biotechnology, National Tsing Hua University, Hsinchu 300044, Taiwan
  4. 4Institute of Molecular Biology, National Chung Hsing University, Taichung 402202, Taiwan
  5. 5School of Dentistry, China Medical University, Taichung 404328, Taiwan
  6. 6Department of Life Science, National Tsing Hua University, Hsinchu 300044, Taiwan
  7. 7School of Medicine, National Tsing Hua University, Hsinchu 300044, Taiwan
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Abstract

Candida albicans is an important human fungal pathogen. Previous studies have shown that the transcription factor Sfp1 is involved in regulation of various biological processes in C. albicans, including cell wall maintenance, biofilm formation, oxidative stress responses, and carbon source adaptation. In this study, we further identified a novel role for Sfp1 in the response to antifungal drugs and virulence. The SFP1 deletion mutant exhibited increased resistance to fluconazole, and this phenotype was associated with altered ergosterol content and enhanced drug efflux pump activity. In addition, the effect of SFP1 deletion on fluconazole resistance was associated with alterations in mitochondrial function and calcium homeostasis. Finally, deletion of the SFP1 gene resulted in attenuated virulence and affected fluconazole efficacy in a mouse model of infection. Together, our study provides new insights into the role of Sfp1 in C. albicans and highlights the complex mechanisms underlying fungal adaptation to antifungal drug stress.

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Cite

BibTeXRIS
BibTeX
@article{huang2026sfp1,
  title = {{Sfp1 Contributes to Fluconazole Responses and Virulence in Candida albicans}},
  author = {Wei-Luen Huang and Hsuan-Yu Chen and Kuo-Yun Tseng and Dinh-Dong Le and Shin-Huey Lin and Yu-Shan Chang and I-Ching Wang and Hsiu-Jung Lo and Chi-Jan Lin and Chung-Yu Lan},
  journal = {International Journal of Molecular Sciences},
  year = {2026},
  month = oct,
  doi = {10.3390/ijms27209206},
  url = {https://www.mdpi.com/1422-0067/27/20/9206},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Sfp1 Contributes to Fluconazole Responses and Virulence in Candida albicans
AU  - Wei-Luen Huang
AU  - Hsuan-Yu Chen
AU  - Kuo-Yun Tseng
AU  - Dinh-Dong Le
AU  - Shin-Huey Lin
AU  - Yu-Shan Chang
AU  - I-Ching Wang
AU  - Hsiu-Jung Lo
AU  - Chi-Jan Lin
AU  - Chung-Yu Lan
PY  - 2026
DA  - 2026/10/16
JO  - International Journal of Molecular Sciences
DO  - 10.3390/ijms27209206
UR  - https://www.mdpi.com/1422-0067/27/20/9206
AB  - Candida albicans is an important human fungal pathogen. Previous studies have shown that the transcription factor Sfp1 is involved in regulation of various biological processes in C. albicans, including cell wall maintenance, biofilm formation, oxidative stress responses, and carbon source adaptation. In this study, we further identified a novel role for Sfp1 in the response to antifungal drugs and virulence. The SFP1 deletion mutant exhibited increased resistance to fluconazole, and this phenotype was associated with altered ergosterol content and enhanced drug efflux pump activity. In addition, the effect of SFP1 deletion on fluconazole resistance was associated with alterations in mitochondrial function and calcium homeostasis. Finally, deletion of the SFP1 gene resulted in attenuated virulence and affected fluconazole efficacy in a mouse model of infection. Together, our study provides new insights into the role of Sfp1 in C. albicans and highlights the complex mechanisms underlying fungal adaptation to antifungal drug stress.
SN  - 1422-0067
ER  -