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N-Acetyl-D-glucosamine-induced germ tube formation in Candda albicans at 37°C was accompanied by an increase in the rate of protein phosphorylation. The calmodulin antagonist trifluoperazine and the Ca2+ ionophore A23187, which inhibited germ tube formation, also reduced the rate of phosphorylation. The rate of phosphorylation was also reduced when cells were incubated at 25 "C, which favoured yeast-phase growth. Twodimensional SDS-PAGE analysis of phosphoproteins from germ-tube-forming and yeast cells revealed two germtube-specific and three yeast-specific phosphoproteins. Germ tubes and hyphae had more calmodulin activity than yeast cells, irrespective of the germ-tube-inducing condition used. As a first step towards understanding the inhibitory effect of trifluoperazine on germ tube formation, calmodulin from C. albicans was purified to homogeneity. It was heat stable, and displayed a pronounced Ca2+-induced shift in electrophoretic mobility.

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Stationary phase cells of Candida albicans are under the control of glucose repression, as indicated by the inhibition of germ tube formation by glucose. This ‘glucose effect’ was absent in starved cells which were derived from similar stationary phase cells. Moreover, starved cells required glucose for germ tube formation, suggesting that it was depletion of energy reserves which was the main factor overriding the ‘glucose repression machinery’ during starvation. High concentration of phosphate in Lee's medium was the reason for the reduced ability of the starved cells to form germ tubes at pH 4.5 (20% of cells compared to 88% at pH 6.8). However, when phosphate was replaced or its concentration reduced, germ tube formation occurred as frequently at pH 4.5 as at pH 6.8. This ‘phosphate effect’ was not observed in stationary phase cells, as they were already repressed by glucose.

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