Fig. 8: Dal81 and Stp2 are key regulators of C. albicans commensalism and pathogenesis.
A C. albicans dal81Δ/Δ and stp2Δ/Δ mutant strains showed defective gastrointestinal colonization compared to wild-type (WT) or DAL81comp. strains. Female C57BL/6 mice (n = 8) were orally gavaged with 108 CFU of indicated strains and colonization was measured in fecal pellets on days 3, 5 and 8 post-inoculations via CFU/g quantification. B The dal81Δ/Δstp2Δ/Δ double mutant exhibited complete colonization failure. Mice (n = 8) were gavaged as in (A), with colonization assessed on day 3. C Dal81 and Stp2 promote gut commensalism in immunosuppressed ICR mice (n = 8/group), inoculated with 1:1 mixtures of WT and dal81Δ/Δ, DAL81comp., or stp2Δ/Δ(1 × 108 CFU total). Strain abundance in inoculum (I) and after recovery from fecal pellets (R) was quantified by strain-specific qPCR. D Deletion of DAL81 or STP2 attenuated C. albicans virulence, with Wild-type DAL81 complementation restoring function. C57BL/6 mice (n = 12) were tail-vein infected with 2 × 105 CFU of indicated strains and survival was monitored at the specified timepoints. E The dal81Δ/Δstp2Δ/Δ double mutant showed complete virulence loss. Mice (n = 8) were infected with 1 × 106 CFU as in (D). F Survival of mice (n = 8) after intravenous (i.v.) challenge with the DAL81m21/dal81Δ mutant. Experiments were repeated twice with similar results. Statistical significance via two-way ANOVA with Tukey’s test (A, C), and one-way ANOVA with Tukey’s test (B). Survival data (D, E) were evaluated by Kaplan-Meier and log-rank (Mantel–Cox) test. ns, not significant. Source data are provided as a Source Data file.
