Abstract:Farnesol, a Candida albicans cell-cell signaling molecule that participates in the control of morphology, has an additional role in protection of the fungus against oxidative stress. In this report, we show that though farnesol induces the accumulation of intracellular ROS, ROS generation is not necessary for the induction of catalase (Cat1)-mediated oxidative stress resistance. Two antioxidants, alpha-tocopherol, and to a lesser extent, ascorbic acid effectively reduced intracellular ROS generation by farnesol, but did not alter farnesol-induced oxidative stress resistance. Farnesol inhibits the Ras1-adenylate cyclase (Cyr1) signaling pathway to achieve its effects on morphology in hypha-inducing conditions, and here we demonstrate that farnesol induces oxidative stress resistance by a similar mechanism. Strains lacking either Ras1 or Cyr1 no longer exhibited increased protection against hydrogen peroxide upon pre-incubation with farnesol. While we also observed the previously reported increase in phosphorylation level of Hog1, a known regulator of oxidative stress resistance, in the presence of farnesol, the hog1/hog1 mutant did not differ from wild-type strains in terms of farnesol-induced oxidative stress resistance. Analysis of Hog1 levels and its phosphorylation state in different mutant backgrounds indicated that mutation of the components of Ras1-adenylate cyclase pathway was sufficient to cause an increase of Hog1 phosphorylation even in the absence of farnesol or other exogenous sources of oxidative stress. This finding indicates the presence of unknown links between these signaling pathways. Our results suggest that farnesol effects on the Ras-adenylate cyclase cascade are responsible for many of the observed activities of this fungal signaling molecule.

Status: Published Type: Journal Article PubMed ID: 20118211

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