Abstract

Candida albicans is a major human fungal pathogen. One of the important features of C. albicans pathogenicity is the ability to form biofilms on mucosal surfaces and indwelling medical devices. Biofilm formation involves complex processes in C. albicans, including cell adhesion, filamentous growth, extracellular matrix secretion and cell dispersion. In this work, we characterized the role of the transcription factor Sfp1, particularly with respect to its function in the regulation of biofilm formation. The deletion of the SFP1 gene enhanced cell adhesion and biofilm formation in comparison to the wild-type strain. Interestingly, the sfp1-deleted mutant also exhibited an increase in the expression of the ALS1, ALS3 and HWP1 genes, which encode adhesin proteins. In addition, Sfp1 was demonstrated to function downstream of the Rhb1-TOR signaling pathway. Bcr1 and Efg1 are transcription factors that are critical for controlling biofilm formation, and Efg1 is also required for hyphal growth. Deleting either the BCR1 or EFG1 gene in the sfp1-null background led to reduced adhesin gene expression. As a result, the bcr1/sfp1 or efg1/sfp1 double deletion mutants exhibited dramatically reduced biofilm formation. The results indicated that Sfp1 negatively regulates the ALS1, ALS3 and HWP1 adhesin genes and that the repression of these genes is mediated by the inhibition of Bcr1 and Efg1.

Highlights

  • Candida albicans is a part of the normal microbial flora and typically inhabits the skin, the mucosal surfaces of the oral cavity, and the gastrointestinal and genitourinary tracts

  • C. albicans orf19.5953 was identified as a promising transcription factor that may function in biofilm formation [21]

  • In the liquid β-gal assay, LexA-Sfp1 activated the lacZ reporter gene even more strongly than LexA-Gcn4 (Fig 1). These results indicate that C. albicans Sfp1 is a transcriptional activator

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Summary

Introduction

Candida albicans is a part of the normal microbial flora and typically inhabits the skin, the mucosal surfaces of the oral cavity, and the gastrointestinal and genitourinary tracts. This organism is an opportunistic pathogen that can cause invasive and life-threatening infections, in immunocompromised patients [1]. A critical feature that is closely related to the ability of C. albicans to cause infections is its ability to form surface-associated microbial communities called biofilms [2,3,4]. C. albicans can form biofilms on biotic or inert surfaces, such as the mucosal epithelia and a variety of indwelling medical devices.

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