Background <p><i>Candida albicans</i> represents the predominant opportunistic fungal pathogen in clinical contexts, with its virulence contingent upon multilayered regulatory networks. <i>CaLrp1</i> (orf19.5067) encodes a conserved Sas10/C1D domain-containing protein, though its precise biological role has remained uncharacterized.</p> Results <p><i>CaLrp1</i> deleted and complemented strains were constructed to systematically investigate its function in <i>C. albicans</i>. Abrogation of <i>CaLrp1</i> 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, <i>CaLrp1</i>-deficient strains displayed restricted proliferative capacity, reduced tissue pathology, and significantly attenuated virulence. Transcriptomic profiling via RNA-seq revealed that <i>CaLrp1</i> 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 <i>Als1</i>, <i>Ece1</i>, and <i>Hwp1</i>—were significantly suppressed, a finding consistent with the phenotypic defects observed on solid substrates.</p> Conclusions <p>Our results establish <i>CaLrp1</i> as a critical regulator of <i>C. albicans</i> morphogenesis and pathogenicity, likely operating via the maintenance of cellular RNA-processing and protein-biosynthetic fidelity.</p>