Abstract

Candida albicans, the major human fungal pathogen, undergoes morphological transition from the budding yeast form to filamentous growth in response to nitrogen starvation. In this study, we identified a new function of GST2, whose expression was required for filamentous growth of C. albicans under nitrogen-limiting conditions. The ΔGst2p showed Gst activity and required response to oxidative stress. The Δgst2 mutant displayed predominantly yeast phase growth in low ammonium media. Such morphological defect of Δgst2 mutants was not rescued by overexpression of Mep2p, Cph1p, or Efg1p, but was rescued by either overexpression of a hyperactive RAS1(G13V) allele or through exogenous addition of cyclic AMP. In addition, the Δgst2 mutants had lower levels of RAS1 transcripts than wild-type cells under conditions of nitrogen starvation. These results were consistent with the Ras1-cAMP pathway as a possible downstream target of Gst2p. These findings suggest that Gst2p is a significant component of nitrogen starvation-induced filamentation in C. albicans.

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