Fig. 7.

Model depicting the herein-described molecular checkpoints of V. cholerae’s amoebal infection cycle. After phagocytosis, V. cholerae cells colonize the CV of A. castellanii trophozoites. The bacteria remain within this replication niche upon amoebal encystation (1). After intra-vacuolar growth, rupture of the vacuole occurs in a Vibrio polysaccharide-dependent manner (2), which releases motile V. cholerae into the cyst’s cytosol (3) where the bacteria proliferate further (4). Lecithinase-mediated membrane permeabilization (5) eventually leads to the lysis of the cyst and the quick release of the motile bacteria (6), which can undergo another round of infection. Defined bacterial mutants are blocked at different checkpoints and, therefore, impaired in the progression of the infection cycle: A, protease-deficient and therefore hemolysis-overactive strain (ΔhapA); B, Vibrio polysaccharide (VPS)-deficient strain (ΔvpsA²⁵); C-D, non-motile strains (ΔflaA and ΔpomB); and E, lecithinase-minus strain (Δlec)