DOI: 10.5176/978-981-08-8119-1_BioTech2011_8
Authors: So-Hyoung Lee, Soon-Chun Chung, Wanki Park, Jiyoung Park, Chan-Hong Ahn and Ki-Bong Oh
Abstract:
The yeast Candida albicans is the most prevalent fungal pathogen in humans. This organism undergoes reversible morphogenetic transitions between a budding yeast form and a filamentous hyphal or pseudohyphal form. This ability is regulated by autoregulatory substances (ARS), such as farnesoic acid and farnesol, which accumulate in the medium as the cells proliferate and result in inhibition of the yeast-to-hypha transition. Many signaling pathways and regulators involved in morphogenetic transition have been identified from intensive investigations, but the molecular networks of ARS remain poorly understood. Here, we show that PHO81, a cyclindependent protein kinase (CDK) inhibitor homolog, controls the inhibition of the yeast-to-hypha transition in response to farnesoic acid. The pho81mutant strain existed exclusively as filaments under favorable yeast growth conditions and was insensitive to inhibition of yeast-to-hypha transition by farnesoic acid and repression of CPH1, EFG1, GAP1, and HWP1 transcription. Furthermore, we identified that PHO81 contributes to the regulation of the Ras1 signaling pathway. The pho81mutant containing a dominantactive variant of Ras1 failed to inhibit filament formation by farnesoic acid, and the pho81mutant showed the increased levels of intracellular GTP-bound Ras1 in vivo, heat-shock sensitivity, and invasive growth. These findings identify PHO81 as a novel
molecule for developmental signaling by the fungus and demonstrate that farnesoic acid controls the Ras signaling pathway via PHO81.
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