Journal
MOLECULAR MICROBIOLOGY
Volume 75, Issue 6, Pages 1337-1354Publisher
WILEY
DOI: 10.1111/j.1365-2958.2009.07003.x
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Funding
- Portuguese grant [POCI/BIA-BCM/57812/2004]
- FCT [SFRH/BD/23503/2005]
- BBSRC [BB/C510391/1]
- Wellcome Trust [080088]
- Fundação para a Ciência e a Tecnologia [SFRH/BD/23503/2005, POCI/BIA-BCM/57812/2004] Funding Source: FCT
- Biotechnology and Biological Sciences Research Council [BB/C510391/1, BB/F00513X/1, BB/F010826/1, BBS/B/06679] Funding Source: researchfish
- BBSRC [BB/F010826/1, BB/F00513X/1] Funding Source: UKRI
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P>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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