BMC microbiology · 2026
A conserved Sas10/C1D domain protein, CaLrp1, is a critical regulator of hyphal development and pathogenicity in Candida albicans.
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Yang Yang, Song Dongxu, Huang Mingjiao, Sun Chaoqin, He Juan, Cai Ruxia, Jin Weiwei, Zhao Na, Guo Guo
Аннотация
BACKGROUND: Candida albicans represents the predominant opportunistic fungal pathogen in clinical contexts, with its virulence contingent upon multilayered regulatory networks. CaLrp1 (orf19.5067) encodes a conserved Sas10/C1D domain-containing protein, though its precise biological role has remained uncharacterized.
RESULTS: CaLrp1 deleted and complemented strains were constructed to systematically investigate its function in C. albicans. Abrogation of CaLrp1 resulted in delayed hyphal induction, a loss of rugose colony morphology, and a pronounced reduction in invasive growth on solid media. Furthermore, the mutant demonstrated impaired epithelial translocation, diminished capacity to damage Caco-2 cells, and enhanced susceptibility to macrophage phagocytosis in vitro. In murine models of gastrointestinal colonization and systemic infection, CaLrp1-deficient strains displayed restricted proliferative capacity, reduced tissue pathology, and significantly attenuated virulence. Transcriptomic profiling via RNA-seq revealed that CaLrp1 deletion induced extensive transcriptional reprogramming, marked by the downregulation of genes implicated in ribosome biogenesis, rRNA processing, energy metabolism, and multiple virulence-associated pathways. Notably, key hyphal development and adhesion genes-including Als1, Ece1, and Hwp1-were significantly suppressed, a finding consistent with the phenotypic defects observed on solid substrates.
CONCLUSIONS: Our results establish CaLrp1 as a critical regulator of C. albicans morphogenesis and pathogenicity, likely operating via the maintenance of cellular RNA-processing and protein-biosynthetic fidelity.
RESULTS: CaLrp1 deleted and complemented strains were constructed to systematically investigate its function in C. albicans. Abrogation of CaLrp1 resulted in delayed hyphal induction, a loss of rugose colony morphology, and a pronounced reduction in invasive growth on solid media. Furthermore, the mutant demonstrated impaired epithelial translocation, diminished capacity to damage Caco-2 cells, and enhanced susceptibility to macrophage phagocytosis in vitro. In murine models of gastrointestinal colonization and systemic infection, CaLrp1-deficient strains displayed restricted proliferative capacity, reduced tissue pathology, and significantly attenuated virulence. Transcriptomic profiling via RNA-seq revealed that CaLrp1 deletion induced extensive transcriptional reprogramming, marked by the downregulation of genes implicated in ribosome biogenesis, rRNA processing, energy metabolism, and multiple virulence-associated pathways. Notably, key hyphal development and adhesion genes-including Als1, Ece1, and Hwp1-were significantly suppressed, a finding consistent with the phenotypic defects observed on solid substrates.
CONCLUSIONS: Our results establish CaLrp1 as a critical regulator of C. albicans morphogenesis and pathogenicity, likely operating via the maintenance of cellular RNA-processing and protein-biosynthetic fidelity.