Abstract

C. albicans is one of the most common fungal pathogens of humans. Important virulence-determining traits include proper cell proliferation and the ability to develop into different cell types, including yeast, pseudohyphae and hyphae. Both of these processes are dependent on environmental cues such as availability and types of nutrients. It is thus important to understand how these cues are sensed and integrated with the machinery that control cell division and development. The TOR pathway plays an important role in mediating environmental conditions in many organisms, and accordingly, TOR kinase is required for cell division and the maintenance of hyphal growth in C. albicans (1). However, the mechanisms by which TOR regulates these processes in the pathogen are not clear. Here, we provide the first characterization of Sfp1p, an orthologue of a major downstream effector of TOR kinase in S. cerevisiae. Deletion of SFP1 in C. albicans resulted in a decrease in cell size, which could be reduced further in the presence of poor carbon source media. The sfp1D/sfp1D cells grew slowly, formed small colonies, and were more sensitive to rapamycin, suggesting that Sfp1p mediates a least part of Tor1p function in C. albicans. Transcription profiles of the deletion strain demonstrated down-regulation of genes involved in ribosome biogenesis, translation, and amino acid synthesis, consistent with a role in the TOR pathway. However, many hyphal-specific genes were upregulated, as well as some genes associated with the opaque cell fate, suggesting additional and novel links with development.