ArticleNature communications2023
Candida albicans exploits N-acetylglucosamine as a gut signal to establish the balance between commensalism and pathogenesis.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 23 citations in OpenAlex.
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- Commensal, pathogen, or passenger? Rethinking the role ofOne health (Amsterdam, Netherlands) · 2025Review
- Molecular Triggers of Yeast Pathogenicity in the Yeast-Host Interactions.Current issues in molecular biology · 2025Review
- Transcription factor RonA-driven GlcNAc catabolism is essential for growth, cell wall integrity, and pathogenicity inMicrobiology spectrum · 2025Article
- N-acetyl-glucosamine primes Pseudomonas aeruginosa for virulence through a type IV pili/cAMP-mediated morphology transition.Nature communications · 2025Article
- Head and Neck Malignancies in Autoimmune Polyendocrine Syndrome Type 1 (APS-1/APECED): A Scoping Review of Molecular Pathogenesis, Clinical Features, and Outcomes.International journal of molecular sciences · 2025Article
- Adaptive evolution ofmBio · 2025Article
- Profilin Pfy1 is critical for cell wall integrity and virulence inMicrobiology spectrum · 2025Article
- Shape-Shifting Mechanisms: Integrative Multi-Omics Insights IntoMycobiology · 2025Review
- The rod cell, a small form ofActa biochimica et biophysica Sinica · 2024Article
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- Subpopulation commensalism promotes Rac1-dependent invasion of single cells via laminin-332.The Journal of cell biology · 2024Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Candida albicans is a benign member of gut microbiota, but also causes life-threatening disseminated infections, suggesting that this fungus commensalism has evolved with retention of virulence traits. Here we reveal that N-acetylglucosamine (GlcNAc) enables C. albicans to balance between commensalism and pathogenesis. Although GlcNAc catabolism is beneficial for commensal growth of C. albicans, deleting GlcNAc sensor-transducer Ngs1 confers enhanced fitness, indicating that GlcNAc signaling is detrimental to commensalism. Interestingly, addition of GlcNAc attenuates commensal fitness of gut-evolved C. albicans but retains its disease-causing potential. We further demonstrate that GlcNAc is a major inducer of hypha-associated transcription in the gut, which represents the key determinant for commensal-pathogenic equilibrium. In addition to yeast-to-hypha morphogenesis, we also identify other factors, including Sod5 and Ofi1, that contribute to the balance. Thus, C. albicans uses GlcNAc to build up a tradeoff between fungal programs supporting commensalism and virulence, which may explain its success as a commensal and pathogen.
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Registered trials
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