Fig 9.

Znf2 mediates the fungal ability to cause fatal diseases in the murine inhalation model of cryptococcosis. (A) Mice were inoculated with 1 × 10⁶ fungal cells intranasally, and survival was monitored for 40 days. There was no statistically significant difference between the wild type and the znf2Δ mutant. The P values were 0.07 for WT/znf2Δ, and <0.001 for WT/ZNF2^oe and ZNF2^oe/znf2Δ. (B) Mice were inoculated with 1 × 10⁶ fungal cells intranasally. At the time of termination, lungs, brains, kidneys, and spleens from six animals per group were dissected and homogenized. Serial dilutions of the homogenized tissue were plated, and CFU were used to determine the organ fungal burden. The short, bold, horizontal lines indicate the medians. No colonies were recovered from a few dissected organs even with all the suspended tissue plated. Because the y axis is log₁₀ of the CFU, “n/a” (not applicable) was used to show them as zero on the bottom of the y axis. The fungal burdens among the wild type, the znf2Δ mutant, and the ZNF2^oe strain were statistically different in the lungs (P < 0.001) and the brain (P = 0.004). There was no statistically significant difference in the kidney (P = 0.874) or in the spleen (P = 0.442).