Calcium dependent exocytosis and endocytosis: novel trafficking pathways revealed by the study of host/pathogen interactions

Abstract

Elevation in cytosolic Ca2+ triggers exocytosis of lysosomes, a process required for trypanosome invasion (1) and the resealing of membrane wounds (2). Interactions of bacteria with host cells also involve activation of the plasma membrane repair response. Permeabilization of phagosome membranes by the type three secretion system of the bacterial pathogen Salmonella triggers early lysosomal fusion and bacterial killing (3). SLO, a bacterial pore‐forming toxin, also triggers Ca2+ dependent lysosomal exocytosis and plasma membrane repair. However, the process responsible for removal of the toxin pores from the plasma membrane is a novel, rapid form of endocytosis that follows the exocytosis of lysosomes (4). Characterization of this injury‐induced form of endocytosis showed that it is triggered by the release of specific lysosomal hydrolases. These new findings demonstrate that calcium dependent exocytosis of lysosomes and endocytosis are functionally linked.This work was supported by the NIH.