The Hog1 MAP kinase controls respiratory metabolism in the fungal pathogen Candida albicans.
Signal transduction pathways mediated by mitogen-activated protein kinases (MAPKs) play crucial roles in eukaryotic cells. In the pathogenic fungus Candida albicans the HOG MAPK pathway regulates the response to external stresses (osmotic and oxidative among others) and is involved in morphogenesis and virulence. We show here that the lack of the Hog1 MAPK increases the sensitivity of this fungus to inhibitors of the respiratory chain. hog1 mutants also show an enhanced basal respiratory rate compared to parental strains, and higher levels of intracellular reactive oxygen species despite an increased expression of detoxifying enzymes. We also demonstrate that although oxidative phosphorylation is essentially unaffected, hog1 mutants have an altered mitochondrial membrane potential. Data indicate that hog1-defective mutants are more dependent on mitochondrial ATP synthesis, probably due to an increased cellular ATP demand. Our results therefore link a MAPK pathway with respiratory metabolism in pathogenic fungi.
Alonso-Monge
Rebeca
R
Departamento de Microbiología II, Facultad de Farmacia, Universidad Complutense de Madrid, Plaza de Ramón y Cajal s/n, E-28040 Madrid, Spain.
Carvaihlo
Sara
S
Departamento de Microbiología II, Facultad de Farmacia, Universidad Complutense de Madrid, Plaza de Ramón y Cajal s/n, E-28040 Madrid, Spain.
Nombela
Cesar
C
Departamento de Microbiología II, Facultad de Farmacia, Universidad Complutense de Madrid, Plaza de Ramón y Cajal s/n, E-28040 Madrid, Spain.
Rial
Eduardo
E
Departamento de Ciencias de Proteínas, Centro de Investigaciones Biológicas, CSIC, Ramiro de Maeztu 9, E-28040 Madrid, Spain.
Pla
Jesús
J
Departamento de Microbiología II, Facultad de Farmacia, Universidad Complutense de Madrid, Plaza de Ramón y Cajal s/n, E-28040 Madrid, Spain.
D000255:Adenosine Triphosphate / Q000378:metabolism; D002176:Candida albicans / Q000187:drug effects / Q000201:enzymology / Q000235:genetics / Q000378:metabolism*; D002177:Candidiasis / Q000382:microbiology*; D002701:Chloramphenicol / Q000494:pharmacology; D004579:Electron Transport / Q000187:drug effects; D005656:Fungal Proteins / Q000235:genetics / Q000378:metabolism*; D053078:Membrane Potential, Mitochondrial; D008928:Mitochondria / Q000235:genetics / Q000378:metabolism; D020928:Mitogen-Activated Protein Kinases / Q000235:genetics / Q000378:metabolism*; D009154:Mutation; D009840:Oligomycins / Q000494:pharmacology; D018384:Oxidative Stress; D010100:Oxygen / Q000378:metabolism
D005656:Fungal Proteins; D009840:Oligomycins; D002701:Chloramphenicol; D000255:Adenosine Triphosphate; D020928:Mitogen-Activated Protein Kinases; D010100:Oxygen