Abstract
Microbial pathogens must compete with the iron-withholding defense systems of their host to acquire this essential nutrient. Here, two high-affinity iron permease genes, CaFTR1 and CaFTR2, were isolated. CaFTR1 expression was induced under iron-limited conditions and repressed when iron supply was sufficient, whereas the expression of CaFTR2 was regulated in a reversed manner. Mutants lacking CaFTR1 but not CaFTR2 exhibited a severe growth defect in iron-deficient medium and were unable to establish systemic infection in mice. Thus, CaFTR1-mediated iron-uptake mechanism constitutes a virulence factor of Candida albicans and may be a target for the development of anti-Candida therapies.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Animals
-
Biological Transport
-
Candida albicans / enzymology*
-
Candida albicans / genetics
-
Candida albicans / growth & development
-
Candida albicans / pathogenicity*
-
Candidiasis / microbiology
-
Carrier Proteins / genetics
-
Carrier Proteins / metabolism
-
Cell Membrane / enzymology
-
Culture Media
-
Ferric Compounds / metabolism
-
Gene Deletion
-
Gene Expression Regulation, Fungal
-
Genes, Fungal
-
Iron / metabolism*
-
Kidney / microbiology
-
Membrane Transport Proteins / chemistry
-
Membrane Transport Proteins / genetics*
-
Membrane Transport Proteins / metabolism*
-
Mice
-
Recombinant Fusion Proteins / metabolism
-
Saccharomyces cerevisiae / genetics
-
Saccharomyces cerevisiae / metabolism
-
Saccharomyces cerevisiae Proteins*
-
Transformation, Genetic
-
Virulence
Substances
-
Carrier Proteins
-
Culture Media
-
FTR1 protein, S cerevisiae
-
Ferric Compounds
-
Membrane Transport Proteins
-
Recombinant Fusion Proteins
-
Saccharomyces cerevisiae Proteins
-
Iron