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Antimicrobial Agents and Chemotherapy, February 2005, p. 584-589, Vol. 49, No. 2
0066-4804/05/$08.00+0 doi:10.1128/AAC.49.2.584-589.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
cDNA Microarray Analysis of Differential Gene Expression in Candida albicans Biofilm Exposed to Farnesol
Ying-Ying Cao,1
Yong-Bing Cao,1
Zheng Xu,1
Kang Ying,2
Yao Li,2
Yi Xie,2
Zhen-Yu Zhu,1
Wan-Sheng Chen,1 and
Yuan-Ying Jiang1*
Department of Pharmacology, School of Pharmacy, Second Military Medical University,1
State Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Science, Fudan University, Shanghai, People's Republic of China2
Received 7 June 2004/
Returned for modification 6 July 2004/
Accepted 22 September 2004
Candida albicans biofilms are structured microbial communities with high levels of drug resistance. Farnesol, a quorum-sensing molecule that inhibits hyphal formation in C. albicans, has been found to prevent biofilm formation by C. albicans. There is limited information, however, about the molecular mechanism of farnesol against biofilm formation. We used cDNA microarray analysis to identify the changes in the gene expression profile of a C. albicans biofilm inhibited by farnesol. Confocal scanning laser microscopy was used to visualize and confirm normal and farnesol-inhibited biofilms. A total of 274 genes were identified as responsive, with 104 genes up-regulated and 170 genes down-regulated. Independent reverse transcription-PCR analysis was used to confirm the important changes detected by microarray analysis. In addition to hyphal formation-associated genes (e.g., TUP1, CRK1, and PDE2), a number of other genes with roles related to drug resistance (e.g., FCR1 and PDR16), cell wall maintenance (e.g., CHT2 and CHT3), and iron transport (e.g., FTR2) were responsive, as were several genes encoding heat shock proteins (e.g., HSP70, HSP90, HSP104, CaMSI3, and SSA2). Further study of these differentially regulated genes is warranted to evaluate how they may be involved in C. albicans biofilm formation. Consistent with the down-regulation of the cell surface hydrophobicity-associated gene (CSH1), the water-hydrocarbon two-phase assay showed a decrease in cell surface hydrophobicity in the farnesol-treated group compared to that in the control group. Our data provide new insight into the molecular mechanism of farnesol against C. albicans biofilm formation.
* Corresponding author. Mailing address: Department of Pharmacology, School of Pharmacy, Second Military Medical University, 325 Guohe Rd., Shanghai 200433, People's Republic of China. Phone: 86-21-25070371. Fax: 86-21-6549-0641. E-mail:
jiangyy{at}smmu.edu.cn.
Antimicrobial Agents and Chemotherapy, February 2005, p. 584-589, Vol. 49, No. 2
0066-4804/05/$08.00+0 doi:10.1128/AAC.49.2.584-589.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
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