AI Article Synopsis
- Candida albicans serves as both a beneficial and pathogenic fungus in humans, with its ability to utilize various carbon sources being crucial for its survival and pathogenicity.
- The study identifies a new gene, MCU1, essential for the utilization of N-acetylglucosamine (GlcNAc), which is located in mitochondria and interacts with several key metabolism-related proteins.
- Deletion of MCU1 not only hampers GlcNAc usage but also affects the utilization of other carbon sources and is necessary for filamentation and virulence in mouse models, marking it as a potential target for antifungal drug development.
Article Abstract
The fungus Candida albicans is both a pathogen and a commensal in humans. The ability to utilize different carbon sources available in diverse host niches is vital for both commensalism and pathogenicity. N-acetylglucosamine (GlcNAc) is an important signaling molecule as well as a carbon source in C. albicans. Here, we report the discovery of a novel gene MCU1 essential for GlcNAc utilization. Mcu1 is located in mitochondria and associated with multiple energy- and metabolism-related proteins including Por1, Atp1, Pet9, and Mdh1. Consistently, inactivating Por1 impaired GlcNAc utilization as well. Deletion of MCU1 also caused defects in utilizing non-fermentable carbon sources and amino acids. Furthermore, MCU1 is required for filamentation in several inducing conditions and virulence in a mouse systemic infection model. We also deleted TGL99 and GUP1, two genes adjacent to MCU1, and found that the gup1/gup1 mutant exhibited mild defects in the utilization of several carbon sources including GlcNAc, maltose, galactose, amino acids, and ethanol. Our results indicate that MCU1 exists in a cluster of genes involved in the metabolism of carbon sources. Given its importance in metabolism and lack of a homolog in humans, Mcu1 could be a potential target for developing antifungal agents.
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| http://dx.doi.org/10.1016/j.fgb.2015.01.006 | DOI Listing |
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