ArticleNature communications2025
Candida albicans Ssy1 is the extracellular sensor of gut microbiota-derived peptidoglycan fragments mediating invasive hyphal growth in the host.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed.
- Structural bases of signal generation and transduction by the SPS amino acid sensor of Saccharomyces cerevisiae.G3 (Bethesda, Md.) · 2026Article
- Avian Candidiasis: A Comprehensive Review of Pathogenesis, Diagnosis, and Control.Veterinary sciences · 2026Review
- Bacterial metabolites induce cell wall remodeling, antifungal resistance, and immune recognition of commensal fungi.Current biology : CB · 2026Article
- Article
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Authors and funding
4 authors.
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Abstract
Gut microbiota-derived peptidoglycan fragments (PGNs) are potent inducers of Candida albicans hyphal growth, a key virulence trait for C. albicans pathogenesis in hosts. Herein, we identify the C. albicans oligopeptide transporter 4 (Opt4) as the long-sought major transporter responsible for internalizing a diverse range of natural PGNs into fungal cells. However, contrary to the conventional view, we reveal that blocking the cellular uptake of PGNs does not prevent C. albicans hyphal growth. Instead, we discover that extracellular sensing of PGNs by C. albicans cell surface protein Ssy1 is essential for activating the downstream cAMP-PKA pathway in hyphal signaling. Importantly, the ssy1Δ/Δ mutant, which is defective in PGN-induced hyphal growth, remains unresponsive to the β-lactam-induced PGN storm in the mouse gut. It predominantly maintains yeast morphology and shows no sign of systemic dissemination. These findings establish Ssy1 as a potential anti-virulence target for preventing PGN-induced invasive growth of C. albicans in hosts.
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Registered trials
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