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Abstract
The lipophilic fungal pathogen Malassezia spp. must acquire long-chain fatty acids (LCFAs) from outside the cell. To clarify the mechanism of LCFA acquisition, we investigated fatty acid uptake by this fungus and identified the long-chain acyl-CoA synthetase (ACS) gene FAA1 in three Malassezia spp.: M. globosa, M. pachydermatis, and M. sympodialis. These FAA1 genes could compensate for the double mutation of FAA1 and FAA4 in Saccharomyces cerevisiae, suggesting that Malassezia Faa1 protein recognizes exogenous LCFAs. MgFaa1p and MpFaa1p utilized a medium-chain fatty acid, lauric acid (C12:0). Interestingly, the ACS inhibitor, triacsin C, affected the activity of the Malassezia Faa1 proteins but not that of S. cerevisiae. Triacsin C also reduced the growth of M. globosa, M. pachydermatis, and M. sympodialis. These results suggest that triacsin C and its derivatives are potential compounds for the development of new anti-Malassezia drugs.
Highlights
Malassezia spp. are basidiomycetous fungi that commonly inhabit the skin and scalp of humans and homothermic animals
18 Malassezia species have been identified, all of which lack fatty acid synthetase (FAS) genes in their genome [5,6]. Because of their inability to synthesize fatty acids de novo, it is necessary for Malassezia species to obtain long-chain fatty acids (LCFAs) from outside the cell, such that most Malassezia spp. are lipid dependent
M. pachydermatis is capable of growth on rich media such as yeast peptone dextrose (YPD) and Sabouraud dextrose agar, and was previously thought to be lipid independent, it was recently reported that M. pachydermatis cannot grow on synthetic media lacking fatty acids
Summary
Malassezia spp. are basidiomycetous fungi that commonly inhabit the skin and scalp of humans and homothermic animals. Several Malassezia species can cause infectious diseases, such as atopic dermatitis, seborrheic dermatitis, and pityriasis versicolor in humans, in immunocompromised individuals. 18 Malassezia species have been identified, all of which lack fatty acid synthetase (FAS) genes in their genome [5,6]. Because of their inability to synthesize fatty acids de novo, it is necessary for Malassezia species to obtain long-chain fatty acids (LCFAs) from outside the cell, such that most Malassezia spp. are lipid dependent. Because rich media contain a small amount of fatty acids, it is assumed that M
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