Parasitophorous vacuole poration precedes its rupture and rapid host erythrocyte cytoskeleton collapse in <i>Plasmodium falciparum</i> egress.

ABSTRACT: In the asexual blood stages of malarial infection, merozoites invade erythrocytes and replicate within a parasitophorous vacuole to form daughter cells that eventually exit (egress) by sequential rupture of the vacuole and erythrocyte membranes. The current model is that PKG, a malarial cGMP-dependent protein kinase, triggers egress, activating malarial proteases and other effectors. Using selective inhibitors of either PKG or cysteine proteases to separately inhibit the sequential steps in membrane perforation, combined with video microscopy, electron tomography, electron energy loss spectroscopy, and soft X-ray tomography of mature intracellular Plasmodium falciparum parasites, we resolve intermediate steps in egress. We show that the parasitophorous vacuole membrane (PVM) is perm

SUBMITTER: Hale VL 

PROVIDER: S-EPMC5380091 | biostudies-literature | 2017 Mar

REPOSITORIES: biostudies-literature