Fig 1. The phenotypes caused by the loss or disruption of RZE1 resemble the ones caused by the deletion of ZNF2.

(A) A diagram of various signals (pheromone and other stimuli) that lead to activation of ZNF2 and consequently filamentation in Cryptococcus. (B) The self-filamentation assay of the wild type XL280, the znf2Δ mutant, the rze1 ^Tn mutant, the rze1Δ mutant, and the complemented strains rze1 ^Tn-pRZE1 and rze1Δ-pRZE1 with the wild type allele of RZE1 integrated at the native locus. Strains were cultured on V8 medium for 4 days. (C) Filamentation assay of unilateral crosses during bisexual mating involving a mutant strain and a wild-type mating partner. The α partner is a mutant in the non-self-filamentous H99 background (the rze1Δ mutant, the mat2Δ mutant, and the znf2Δ mutant). The a partner is the wild type KN99a that is congenic with H99. Cells were cultured on V8 medium for about 2 weeks. (D) Confrontation assay with the P_GPD1-CFL1 strain as the donor and the wild type XL280, the rze1Δ mutant, or the znf2Δ mutant as the recipient. (E) Fungal burden analysis from lungs of mice inoculated with the rze1Δ mutants and the corresponding wild-type strains. p = 0.0429 for H99 background and 0.0716 for XL280 background.