Regulation of filamentation in the human fungal pathogenCandida tropicalis

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Abstract

The yeast–filament transition is essential for the virulence of a variety of fungi that are pathogenic to humans. N-acetylglucosamine (GlcNAc) is a potent inducer of filamentation inCandida albicansand thermally dimorphic fungi such asHistoplasma capsulatumandBlastomyces dermatitidis. However, GlcNAc suppresses rather than promotes filamentation inCandida tropicalis, a fungal species that is closely related toC. albicans. Despite the intensive study inC. albicans, the regulatory mechanism of filamentation is poorly understood. In this study, we demonstrate that the cAMP signaling pathway plays a central role in the regulation of filamentation inC. tropicalis. By screening an overexpression library of 156 transcription factors, we have identified approximately 40 regulators of filamentous growth. Although most of the regulators (e.g., Tec1, Gat2, Nrg1, Sfl1, Sfl2 and Ash1) demonstrate a conserved role in the regulation of filamentation, similar to their homologues inC. albicansorSaccharomyces cerevisiae, a number of transcription factors (e.g., Wor1, Bcr1, Stp4, Efh1, Csr1 and Zcf17) play a specific role inC. tropicalis. Our findings indicate that multiple interconnected signaling pathways are involved in the regulation of filamentation inC. tropicalis. These mechanisms have conserved and divergent features among differentCandidaspecies.

The ability to undergo filamentation is essential for the virulence of many pathogenic fungi. N-acetylglucosamine (GlcNAc) suppresses filamentous growth inCandida tropicalis, a related species of the major human fungal pathogenCandida albicans. We characterize the cAMP signaling pathway and a number of transcription factors in the regulation of filamentation inC. tropicalis. The conserved and divergent features of the regulatory mechanism reflect differences in ecological niches betweenC. albicansandC. tropicalis.

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