Cited by 64Fungal and yeast genetics researchAntifungal resistance and susceptibilityFungal Infections and Studies

Functional specialization and differential regulation of short‐chain carboxylic acid transporters in the pathogen Candida albicans

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Vieira, Neide, Casal, Margarida, Johansson, Björn, MacCallum, Donna M., Brown, Alistair J.P., Paiva, Sandra·2010·Molecular Microbiology

Abstract

The major fungal pathogen Candida albicans has the metabolic flexibility to assimilate a wide range of nutrients in its human host. Previous studies have suggested that C. albicans can encounter glucose-poor microenvironments during infection and that the ability to use alternative non-fermentable carbon sources contributes to its virulence. JEN1 encodes a monocarboxylate transporter in C. albicans and we show that its paralogue, JEN2, encodes a novel dicarboxylate plasma membrane transporter, subjected to glucose repression. A strain deleted in both genes lost the ability to transport lactic, malic and succinic acids by a mediated mechanism and it displayed a growth defect on these substrates. Although no significant morphogenetic or virulence defects were found in the double mutant strain, both JEN1 and JEN2 were strongly induced during infection. Jen1-GFP (green fluorescent protein) and Jen2-GFP were upregulated following the phagocytosis of C. albicans cells by neutrophils and macrophages, displaying similar behaviour to an Icl1-GFP fusion. In the murine model of systemic candidiasis approximately 20-25% of C. albicans cells infecting the kidney expressed Jen1-GFP and Jen2-GFP. Our data suggest that Jen1 and Jen2 are expressed in glucose-poor niches within the host, and that these short-chain carboxylic acid transporters may be important in the early stages of infection.

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Crossref · 10.1111/j.1365-2958.2009.07003.x

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  • This hypothesis was supported by the apparent expression regulation of two C. albicans carboxylic acids transporter genes, JEN1 and JEN2, following macrophages internalization.

    “This hypothesis was supported by the apparent expression regulation of two C. albicans carboxylic acids transporter genes, JEN1 and JEN2, following macrophages internalization.”

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Authors
Vieira, N., Casal, M., Johansson, B., MacCallum, D. M., Brown, A. J. P., & Paiva, S.
Affiliations
  • University of Minho (PT)
  • University of Aberdeen (GB)
Corresponding author
Paiva, Sandra
Venue
Molecular Microbiology
Publisher
Wiley
Published
2010-03
Volume
75
Issue
6
Pages
1337-1354
ISSN
  • 0950-382X (ISSN-L)
  • 1365-2958
OpenAlex
W1980561427
Cited by
63
References
80
Citations by year
2026: 2 · 2025: 5 · 2024: 3 · 2023: 4 · 2022: 6 · 2021: 5 · 2020: 6 · 2019: 3 · 2018: 4 · 2017: 5 · 2016: 2 · 2015: 3 · 2014: 4 · 2012: 5
FWCI
1.47
Type
journal article
Language
en
Open access
Locations
  • Molecular Microbiology (publishedVersion)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Aberdeen University Research Archive (Aberdeen University) (submittedVersion)
Funders
  • Wellcome Trust (080088)
  • Biotechnology and Biological Sciences Research Council (BBS/B/06679, BB/C510391/1, BB/F00513X/1, BB/F010826/1)
  • Fundação para a Ciência e a Tecnologia
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
  • Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
  • Health Sciences › Medicine › Epidemiology › Fungal Infections and Studies
Keywords
Candida albicans, dicarboxylate transporter, monocarboxylate transporters, glucose repression, non-fermentable carbon sources, systemic candidiasis, host-pathogen interaction, neutrophil phagocytosis, macrophages, lactic acid, malic acid, succinic acid, virulence
MeSH terms
Animals, Candida albicans, Candidiasis, Carboxylic Acids, Fungal Proteins, Macrophages, Neutrophils, Phagocytosis, Recombinant Fusion Proteins, Survival Analysis, Gene Deletion, Genes, Reporter, Artificial Gene Fusion, Gene Expression Profiling, Membrane Transport Proteins, Green Fluorescent Proteins, Mice

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