Study on the functions of ERG3 in Candida albicans
10.12206/j.issn.2097-2024.202505044
- VernacularTitle:白念珠菌ERG3基因功能研究
- Author:
Zi YE
1
;
Ruina WANG
1
;
Jiacun LIU
2
;
Shiyun YANG
1
;
Chan LIANG
1
;
Lan YAN
1
Author Information
1. Military Special Drug Research Center，School of Pharmacy/Center for Basic Research and Innovation of Medicine and Pharmacy, Naval Medical University, Shanghai 200433, China.
2. No.92880 Hospital of PLA, Zhoushan 316000, China.
- Publication Type:Originalarticles
- Keywords:
Candida albicans;
sterol biosynthesis pathway;
C-5 desaturase
- From:
Journal of Pharmaceutical Practice and Service
2025;43(9):431-435
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the biological functions of the ERG3 gene in Candida albicans and its potential value in antifungal therapy. Methods The ERG3 null mutant was constructed by the CRISPR/Cas9 technology. Gas chromatography-mass spectrometry, microbroth dilution method, hyphal induction and mouse systemic infection models were carried out to evaluate sterol metabolism, drug susceptibility, hyphal formation ability and pathogenicity in C. albicans. Results The disruption of the ERG3 gene led to disordered sterol metabolism in C. albicans with a significant increased level of episterol, 14α-methylfecosterol and ergosta-7,22-dienol. The ERG3 null mutant exhibited significantly reduced susceptibility to antifungal azole and polyene drugs, which suggested that ERG3 involve in regulating drug resistance. Although the disruption of ERG3 inhibited hyphal growth and biofilm formation, it did not significantly alter the pathogenicity of the strain in a mouse model of systemic fungal infection. Conclusion The ERG3 gene was a key regulator in the ergosterol synthesis pathway in C. albicans. Its deletion induced multi-drug resistance by reshaping sterol metabolism, while pathogenicity maintenance depended on compensatory mechanisms. This study provided critical insights for developing antifungal drugs targeting sterol metabolism and overcoming drug resistance.
