Calcium transport and the growth and morphogenesis of Candida albicans
The aim of this study was to investigate the role of Ca2+ signalling pathways in the growth, morphogenesis and hyphal reorientation responses of C. albicans. The genes CCH1 and MID1 were identified in S. cerevisiae as encoding putative Ca2+ channels. These genes have since been shown to compose a Ca2+ channel complex. Homologues of these genes were identified and cloned from C. albicans. CaMID1 was disrupted by the Ura-blaster method, and the resulting mutant characterised. The C. albicans mid1 mutant strain was sensitive to the depletion of Ca2+ the presence of cell wall perturbing compounds such as SDS and Calcofluor. It formed hyphae more rapidly in the presence of serum, and had a propensity to grow as elongated cells or pseudohyphae in Ca2+-depleted medium, on SD, or on medium containing cell wall perturbing compounds. This suggests that depletion of Ca2+-uptake perturbs yeast-hypha morphogenesis, perhaps by inducing a nutrient starvation stress response. The mid1 mutant and a number of other C. albicans Ca2+ signalling mutants were defective in chlamydospore formation, suggesting a role for Ca2+ in two morphogenetic genesises: the hyphae and of chlamydospores. The role of Mid1p in the thigmotropic reorientation responses of C. albicans hyphae was investigated. The mid1 mutant strain displayed reduced ability to reorientate growth upon contact with ridges on an etched quartz slide. Suggesting that Mid1p may function as stretch-activated Ca2+ channel in C. albicans. The ability of C. albicans mid1 mutants to respond to an electric field was also attenuated, suggesting that Mid1p may form part of a voltage-sensitive Ca2+ channel in C. albicans that plays a central role in the steering mechanism of C. albicans hyphae. The C. albicans kinase Cst20p may function downstream of Mid1p in growth reorientation responses.