Fungi from the genus Candida are common members of the human microbiota; however, they are also important opportunistic pathogens in immunocompromised hosts. Several morphological transitions have been linked to the ability of these fungi to occupy the different ecological niches in the human body. The transcription factor Efg1 from the APSES family plays a central role in the transcription circuits underlying several of these morphological changes. In Candida albicans, for example, Efg1 is a central regulator of filamentation, biofilm formation, and white-opaque switching, processes associated with survival in the human host. Orthologs of Efg1 are present throughout the Candida clade but, surprisingly, the genome sequence of Candida tropicalis failed to uncover a gene coding for Efg1. One possibility was that the paralog of Efg1, Efh1, had assumed the function of Efg1 in C. tropicalis. However, we show that this gene has only a minor role in the morphological transitions mentioned above. Instead, we report here that C. tropicalis does have an ortholog of the EFG1 gene found in other Candida species. The gene is located in a different genomic position than EFG1 in C. albicans, in a region that contains a gap in the current genome assembly of C. tropicalis. We show that the newly identified C. tropicalis EFG1 gene regulates filamentation, biofilm formation, and white-opaque switching. Our results highlight the conserved role of Efg1 in controlling morphogenesis in Candida species and remind us that published genome sequences are drafts that require continuous curation and careful scrutiny.
Keywords: Candida morphogenesis; biofilm; filamentation; phenotypic switch; transcriptional regulation.
Copyright © 2015 Mancera et al.