Abstract
Bacteria-host interactions are characterized by the delivery of bacterial virulence factors, i.e., effectors, into host cells where they counteract host immunity and exploit host responses allowing bacterial survival and spreading. These effectors are translocated into host cells by means of dedicated secretion systems such as the type 3 secretion system (T3SS). A comprehensive understanding of effector translocation in a spatio-temporal manner is of critical importance to gain insights into an effector’s mode of action. Various approaches have been developed to understand timing and order of effector translocation, quantities of translocated effectors and their subcellular localization upon translocation into host cells. Recently, the existing toolset has been expanded by newly developed state-of-the art methods to monitor bacterial effector translocation and dynamics. In this review, we elaborate on reported methods and discuss recent advances and shortcomings in this area of tracking bacterial effector translocation.
Highlights
Gram-positive bacteria, such as Listeria monocytogenes (L. monocytogenes), usually deliver their effectors via general secretion systems, including the conserved Sec secretion system found in all classes of bacteria in which unfolded proteins harboring an N-terminal signal peptide are translocated across the membrane [1]
Effector secretion is more challenging for diderm (Gram-negative) bacteria as effectors have to be translocated across two membranes, i.e., the inner and outer membrane, or even three membranes in the context of infection during which effectors are translocated across the host cell membrane
As such, unfolded proteins–prevented from folding by chaperones to maintain a secretion-compatible conformation–can pass from the bacterial cytoplasm through the inner hollow core of the needle into the extracellular space or into the host cell [11]. The latter is enabled by the translocon–a structure consisting of translocators which are substrates of the type 3 secretion system (T3SS)–that is assembled onto the translocator assembly platform and inserted into the host cell membrane immediately upon host cell contact [12]
Summary
To optimize bacterial survival, replication and dissemination, pathogens evolved a myriad of mechanisms to counteract or deceive host immune surveillance systems and to exploit host responses In part, this is achieved by the translocation of (proteinaceous) virulence factors–designated as effectors–into host cells by means of dedicated secretion systems. As such, unfolded proteins–prevented from folding by chaperones to maintain a secretion-compatible conformation–can pass from the bacterial cytoplasm through the inner hollow core of the needle into the extracellular space or into the host cell [11] The latter is enabled by the translocon–a structure consisting of translocators which are substrates of the T3SS–that is assembled onto the translocator assembly platform and inserted into the host cell membrane immediately upon host cell contact [12]. T3Es direct the early biogenesis of the Salmonella-containing vacuole (SCV), SPI-2 T3Es are responsible for the subsequent SCV maturation, intracellular bacterial survival, and direction of the systemic phase of infection [22]
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