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Candida albicans , a prevailing opportunistic fungal pathogen of humans, has a diploid genome containing three homologousFKS genes that are evolutionarily conserved. One of these, the essential geneFKS1 , encodes the catalytic subunit of glucan synthase, which is the target of echinocandin drugs and also serves as a site of drug resistance. The other two glucan synthase-encoding genes,FKS2 andFKS3 , are also expressed, but their roles in resistance are considered unimportant. However, we report here that expression ofFKS1 is upregulated in strains lacking eitherFKS2 orFKS3 . Furthermore, in contrast to what is observed in heterozygousFKS1 deletion strains, cells lackingFKS2 orFKS3 contain increased amounts of cell wall glucan, are more resistant to echinocandin drugs, and consistently are tolerant to cell wall-damaging agents. Our data indicate thatC. albicans FKS2 andFKS3 can act as negative regulators ofFKS1 , thereby influencing echinocandin susceptibility.

FKS2 and FKS3 Genes of Opportunistic Human Pathogen Candida albicans Influence Echinocandin Susceptibility