AbstractThe relationship between the morphology and virulence of Candida albicans has aroused interest in the study of the proteins involved in its morphogenesis. We present virulence data for one important element in fungal morphogenesis—septins. We disrupted CaCDC10 and studied the virulence in a mouse infection model and the different steps followed by the fungus during the infection: adherence to epithelial cells, organ colonisation, macrophage phagocytosis, and host survival. We found the altered subcellular localisation of Int1—a C. albicans adhesin— in the septin null mutants. The Int1 mislocalisation and the defects in the cell wall of defective CaCdc10 strains permit us to propose a model for explaining the biological meaning of the absence of virulence presented by these septin mutants.