Candida albicans is a yeast-like pathogen known to cause serious infections in immunocompromised patients. It has been recognized as the fourth most common cause of blood stream infection among hospitalized patients. The species occurs in two distinct biotypes differentiated by their ability to assimilate sucrose. The strains unable to assimilate sucrose and thus identified as C. albicans var. stellatoidea has been known to have reduced virulence in animal models compared to the type variety. Moreover, previous studies revealed that the stellatoidea variety has a slower growth rate, higher sensitivity to ultraviolet irradiation than the type variety and is unable to assimilate glycerol. Rarely, a sucrose positive revertant occurs and these characteristics co-convert with the sucrose marker. This phenomenon suggested that C. albicans var. stellatoidea had a mutation in a global regulatory gene. The sucrose negative phenotype is itself unrelated to virulence of Candida albicans since a Suc- strain due to a mutation in the casuc1 gene and its Suc+ revertant have equal degrees of virulence in mice. Sucrose utilization, however, appears to be a useful marker for the study of a regulatory pathway shared by cellular processes pertinent to C. albicans as a pathogen. The SNF1 gene, first isolated from S. cerevisiae, encodes a serine/threonine protein kinase which is essential for the removal of catabolic repression. In the previous year,we have cloned the SNF1 gene from C. albicans and showed that it complemented the Suc- phenotype of S. cerevisiae. We also showed that the gene is recessive since the heterozygote, SNF1/snf1, had a Suc+ phenotype. In this study, we attempted to disrupt both alles and showed evidence that SNF1 is an essential gene for viability of C. albicans. This indicate that SNF1 in C. albicans has additional roles in cell biology than the SNF1 gene in S. cerevisiae.
