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interest The authors declare that no competing interests exist. Authors’ contributions AC and RVH designed the study; contributed to the mTOR inhibitor acquisition, analysis and interpretation of data, and wrote the manuscript. BL and RW performed proteomic analysis and data interpretation. AA assisted in data interpretation and contributed to manuscript writing. PC
contributed to data interpretation, and NL helped to draft the manuscript. All authors read and approved Tryptophan synthase the final manuscript.”
“Background Candida albicans is an opportunistic human pathogen and the leading cause of a wide range of human fungal infections. C. albicans is a polymorphic fungus and either grows as a unicellular budding yeast cell or in a filamentous, (pseudo)hyphal form, depending on environmental conditions, such as temperature, pH or presence of chemical stimuli such as serum components or N-acetylglucosamine [1–3]. The ability to switch between different morphologies is important for C. albicans virulence [4, 5]. It is presumed that yeast cells facilitate dissemination to target organs, whereas hyphae play a role in further tissue invasion due to the ability to adhere to and pierce host epithelial and endothelial cells, damaging them through the release of hydrolytic enzymes and initiate candidiasis [5–7]. C. albicans morphological plasticity also plays an important role in biofilm formation and maturation. C. albicans mutants unable to perform morphological switches can develop only rudimentary biofilms, that are structurally less stable than wild type biofilms [8–10]. C. albicans co-exists with a highly diverse bacterial flora in various sites of the human body, resulting in mixed species biofilms [11, 12].