Abstract
During the intracellular life of Salmonella enterica, a unique membrane-bound compartment termed Salmonella-containing vacuole, or SCV, is formed. By means of translocated effector proteins, intracellular Salmonella also induce the formation of extensive, highly dynamic membrane tubules termed Salmonella-induced filaments or SIF. Here we report the first detailed ultrastructural analyses of the SCV and SIF by electron microscopy (EM), EM tomography and live cell correlative light and electron microscopy (CLEM). We found that a subset of SIF is composed of double membranes that enclose portions of host cell cytosol and cytoskeletal filaments within its inner lumen. Despite some morphological similarities, we found that the formation of SIF double membranes is independent from autophagy and requires the function of the effector proteins SseF and SseG. The lumen of SIF network is accessible to various types of endocytosed material and our CLEM analysis of double membrane SIF demonstrated that fluid phase markers accumulate only between the inner and outer membrane of these structures, a space continual with endosomal lumen. Our work reveals how manipulation of the endosomal membrane system by an intracellular pathogen results in a unique tubular membrane compartmentalization of the host cell, generating a shielded niche permissive for intracellular proliferation of Salmonella.
Highlights
Bacterial pathogens have evolved sophisticated mechanisms to modify host cell functions in order to avoid antimicrobial defense or to use host cell-derived material for their own proliferation
We report that Salmonella-induced tubules (SIT) emerge as single membrane tubules that convert into double membrane tubules entrapping cytosol and cytoskeletal filaments
Labeling of the endosomal compartment and cytochemistry demonstrate that the space between inner and outer SIT membrane is composed of internalized material and connected to Salmonella within the Salmonella-containing vacuole (SCV)
Summary
Bacterial pathogens have evolved sophisticated mechanisms to modify host cell functions in order to avoid antimicrobial defense or to use host cell-derived material for their own proliferation. Intracellular pathogens evade humoral immune responses of the host by hiding inside cells of the host organism, using these cells to support their own proliferation and to disseminate within the host organism [1]. These activities require the manipulation of the normal host cell processes to avoid killing by the host cell and to establish a replication-permissive intracellular niche. Salmonella enterica is a facultative intracellular pathogen that modifies eukaryotic host cells in order to establish a unique parasitophorous vacuole, the Salmonella-containing vacuole or SCV [2,3]. One unique phenotype resulting from these interactions is the induction of long tubular membrane compartments extending from the SCV, termed Salmonellainduced filaments or SIF [8]
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