Fig 1.
Mitochondrial-associated activities that impact fungal pathogenesis.
Mitochondria play key roles in stress responses and metabolic activities (e.g., iron homeostasis and use of carbon sources) relevant to fungal proliferation in mammalian hosts. Recent studies emphasize the prominent participation of the ETC in virulence, and the targets of inhibitors of specific complexes are shown in Fig 2. The phenotypic outcomes of perturbed mitochondrial function include cell surface changes that directly influence evasion of the host immune response. Critically important activities related to drug susceptibility and resistance are the subject of other recent reviews [2–9]. cAMP, cyclic adenosine monophosphate; ETC, electron transport chain; PKA, protein kinase A; ROS, reactive oxygen species.
Fig 2.
Inhibitors of ETC components provoke a variety of responses in fungal pathogens.
A schematic illustrating the respiratory chain protein complexes in the inner mitochondrial membrane is shown along with the inhibitors that target specific complexes, as highlighted in the text. Selected examples of the key phenotypic responses to the inhibitors are indicated on the right. Note that capsule formation is specific to C. neoformans. ETC, electron transport chain; SHAM, salicylhydroxamic acid; SNP, sodium nitroprusside.