Ops Normal: a novel protein sequestration sequence to prevent a phenotypic switch in Candida albicans

Candida albicans is a fungus that, despite being considered part of normal human flora, has the potential to cause life-threatening systemic infections, with candida infections being the fourth leading cause of hospital acquired systemic infections and resulting in mortality rates of up to 50%. Candida albicans becomes pathogenic after a phenotype switch from white-to-opaque or opaque-to-white, depending on the infection site. Here, we cloned the 5’ UTR of the master white-opaque phenotypic regulator WOR1 into a vector to act as a protein sequestration sequence. To confirm successful cloning of the 5’ UTR and expression of our vector, we used E. coli as our model organism. Once integrated into the Candida albicans genome, our genetically engineered part should sequester transcriptional regulating proteins away from the WOR1 gene and alter the phenotypic switching tied to the pathogenicity of Candida albicans.