Antifungal activity of plant defensin AFP1 in Brassica juncea involves the recognition of the methyl residue in glucosylceramide of target pathogen Candida albicans

An antifungal defensin, AFP1, of Brassica juncea inhibits the growth of various microorganisms. The molecular details of this inhibition remain largely unknown. Herein, we reveal that a specific structure of fungal sphingolipid glucosylceramide (GlcCer) is critical for the sensitivity of Candida alb...

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Bibliographic Details
Published in:Current genetics 2014-05, Vol.60 (2), p.89-97
Main Authors: Oguro, Yoshifumi, Yamazaki, Harutake, Takagi, Masamichi, Takaku, Hiroaki
Format: Article
Language:English
Subjects:
Antifungal Agents - metabolism
antifungal properties
Biochemistry
Biomedical and Life Sciences
Brassica juncea
Candida albicans
Candida albicans - drug effects
Candida albicans - pathogenicity
Cell Biology
cell viability
Defensins - genetics
Defensins - metabolism
Glucosylceramides - genetics
Glucosylceramides - metabolism
Life Sciences
Microbial Genetics and Genomics
Microbiology
Microorganisms
Mustard Plant - genetics
Mustard Plant - growth & development
Pathogens
Plant Diseases - genetics
Plant Sciences
plasma membrane
Proteomics
reactive oxygen species
Reactive Oxygen Species - metabolism
Research Article
Yeasts
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Summary:An antifungal defensin, AFP1, of Brassica juncea inhibits the growth of various microorganisms. The molecular details of this inhibition remain largely unknown. Herein, we reveal that a specific structure of fungal sphingolipid glucosylceramide (GlcCer) is critical for the sensitivity of Candida albicans cells to AFP1. Our results revealed that AFP1 induces plasma membrane permeabilization and the production of reactive oxygen species (ROS) in wild-type C. albicans cells, but not in cells lacking the ninth methyl residue of the GlcCer sphingoid base moiety, which is a characteristic feature of fungi. AFP1-induced ROS production is responsible for its antifungal activity, with a consequent loss of yeast cell viability. These findings suggest that AFP1 specifically recognizes the structural difference of GlcCer for targeting of the fungal pathogens.
ISSN:0172-8083
1432-0983
DOI:10.1007/s00294-013-0416-8