Mechanisms by which hypoxia induces β-glucan masking in C. albicans. Combining our observations with those of others, we propose the following working model. Hypoxia triggers an increase in the formation of mitochondrial superoxide by the respiratory apparatus (57, 58). Inactivating Goa1 or Upc2, which promote mitochondrial functionality, reduces overall respiration rates and hence mitochondrial ROS production. The alternative oxidase (Aox1) acts to limit mitochondrial ROS production (60–62) and therefore inactivating Aox1 enhances the signal. Superoxide dismutase within the mitochondrial inner membrane space (IMS) converts superoxide into diffusible hydrogen peroxide, which leads to the generation of a mitochondrial signal that transduces to the cytoplasm (see text). This possibly leads to the activation of adenylyl cyclase (Cyr1) and cAMP-PKA (Tpk1/2) signaling, which triggers remodelling of the cell wall and masking of cell surface β-glucan by mechanisms that remain to be elaborated.