Abstract
Candida albicans is the most common human fungal pathogen, causing not only superficial infections, but also life-threatening systemic disease. C. albicans can grow in several morphological forms including unicellular yeast-form, elongated hyphae and pseudohyphae. In certain natural environments, C. albicans also exists as biofilms, which are structured and surface-attached microbial communities. Transcription factors play a critical role in morphogenesis and biofilm development. In this study, we identified four adhesion-promoting transcription factors (Tec1, Cph1, Ume6 and Gat2) by screening a transcription factor overexpression library. Sequence analysis indicates that Gat2 is a GATA-type zinc finger transcription factor. Here we showed that the gat2/gat2 mutant failed to form biofilms on the plastic and silicone surfaces. Overexpression of GAT2 gene promoted filamentous and invasive growth on agar containing Lee's medium, while deletion of this gene had an opposite effect. However, inactivation of Gat2 had no obvious effect on N-acetyl-glucosamine (GlcNAc) induced hyphal development. In a mouse model of systemic infection, the gat2/gat2 mutant showed strongly attenuated virulence. Our results suggest that Gat2 plays a critical role in C. albicans biofilm formation, filamentous growth and virulence.
Highlights
Candida albicans is the most common human fungal pathogen
Since the roles of Cph1, Ume6 and Tec1 in morphogenesis and biofilm formation have been intensively investigated, in this study we focused on the biological roles of Gat2, a GATA-type zinc finger transcription factor
Screen for the adhesion-promoting transcription factors C. albicans biofilm development includes a series of sequential steps: adherenceRinitiationRmaturationRdispersal [10]
Summary
Candida albicans is the most common human fungal pathogen. With the increase in the number of immunocompromised patients, Candida infection is becoming more and more serious worldwide. C. albicans causes superficial infections, and lifethreatening systemic disease in immunocompromised hosts [1,2]. C. albicans can grow in several morphological forms including unicellular yeast-form, elongated hyphae and pseudohyphae. A variety of external and internal factors have been shown to regulate morphogenetic transition in this yeast. The addition of inducers such as serum and N-acetylglucosamine (GlcNAc) and increases in temperature and pH can promote filamentous growth [4]. C. albicans morphogenesis is regulated by a number of signal transduction pathways as well as a number of key regulators such as kinases and zinc finger transcription factors. The cAMP/PKA mediated pathway and the Cst20-Ste11-Hst7-Cph pathway, have been intensively investigated [2,5,6,7,8]
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