Author(s): Bezerra, Ana Rita ; Oliveira, Carla ; Correia, Inês ; Guimarães, Ana Rita ; Sousa, Gonçalo ; Carvalho, Maria João ; Moura, Gabriela ; Santos, Manuel A. S.
Date: 2021
Persistent ID: http://hdl.handle.net/10773/34661
Origin: RIA - Repositório Institucional da Universidade de Aveiro
Subject(s): Candida albicans; Drug resistance; Evolution; Genetic diversity; Non-standard translation; Pathogenesis
Candida albicans typically resides in the human gastrointestinal tract and mucosal membranes as a commensal organism. To adapt and cope with the host immune system, it has evolved a variety of mechanisms of adaptation such as stress-induced mutagenesis and epigenetic regulation. Niche-specific patterns of gene expression also allow the fungus to fine-tune its response to specific microenvironments in the host and switch from harmless commensal to invasive pathogen. Proteome plasticity produced by CUG ambiguity, on the other hand is emerging as a new layer of complexity in C. albicans adaptation, pathogenesis, and drug resistance. Such proteome plasticity is the result of a genetic code alteration where the leucine CUG codon is translated mainly as serine (97%), but maintains some level of leucine (3%) assignment. In this review, we dissect the link between C. albicans non-standard CUG translation, proteome plasticity, host adaptation and pathogenesis. We discuss published work showing how this pathogen uses the fidelity of protein synthesis to spawn novel virulence traits.
