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. Candida infections are the fourth leading cause of hospital acquired systemic infections and result in mortality rates of up to 7.1%.1,2 Candida albicans becomes pathogenic after a phenotype switch from white-to-opaque or opaque-to-white, depending on the infection site. The USAFA iGEM team 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, the team 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 transcript and alter the phenotypic switching tied to the pathogenicity of Candida albicans.


  • 1. Blyth, Dana M., et al. "Resistance patterns and clinical significance of Candida colonization and infection in combat-related injured patients from Iraq and Afghanistan." Open forum infectious diseases. Vol. 1. No. 3. Oxford University Press, 2014.
  • 2. Tribble, David R., et al. "Infection-associated clinical outcomes in hospitalized medical evacuees following traumatic injury-Trauma Infectious Disease Outcome Study (TIDOS)." The Journal of trauma 71.1 0 (2011): S33.