Abstract
Salmonellae are bacteria that cause moderate to severe infections in humans, depending on the strain and the immune status of the infected host. These pathogens have the particularity of residing in the cells of the infected host. They are usually found in a vacuolar compartment that the bacteria shape with the help of effector proteins. Following invasion of a eukaryotic cell, the bacterial vacuole undergoes maturation characterized by changes in localization, composition and morphology. In particular, membrane tubules stretching over the microtubule cytoskeleton are formed from the bacterial vacuole. Although these tubules do not occur in all infected cells, they are functionally important and promote intracellular replication. This review focuses on the role and significance of membrane compartment remodeling observed in infected cells and the bacterial and host cell pathways involved.
Highlights
There are two species of Salmonella (S. enterica and S. bongori) but the strains that are pathogenic to humans almost always belong to the species enterica, which is subdivided into six subspecies and a large number of serotypes
This review illustrates the importance of type 3 secretion system (T3SS) effectors in the tailoring and maintenance of the membrane constituting the intracellular replicative niche and more that of SifA
This T3SS-2 effector is a pillar that allows the anchoring of host proteins which, in turn, possess multiple interactors capable of regulating the membrane dynamics of Salmonellacontaining vacuole (SCV) and Salmonella-induced tubules (SIT)
Summary
There are two species of Salmonella (S. enterica and S. bongori) but the strains that are pathogenic to humans almost always belong to the species enterica, which is subdivided into six subspecies and a large number of serotypes. In Salmonella infected cells, the T3SS-2 effector SifA, present on the surface of SCVs, sequesters Rab9. Tubules that have the distinctive feature of being largely devoid of host proteins can be observed in cells infected with a strain that expresses neither SifA nor SopD2, another effector of T3SS2.
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