There are many methods used to identify effector proteins and to probe how they mediate the host-pathogen interface. Therefore, innovative techniques have emerged to shed light on effector protein translocation and localization within the host cell in order to illuminate how they modulate the host cell during infection (Figure 1). By determining the specific roles of these essential effector proteins in generating and sustaining an intracellular niche for bacteria, we can better understand the virulence of Salmonella and other Enterobacteriaceae. While effector proteins are essential for enabling pathogens to establish successful infection, in many cases the functions of individual effectors and exactly how effectors promote infection are not completely understood. On the other hand, the vacuolar population that persists within the SCV switch to SPI-2 expression in order to maintain intracellular life. Following internalization, a subset of bacteria is able to escape the SCV ( Knodler et al., 2014) and this unique cytosolic population continues to express T3SS-1 late into infection delivering SPI-1 effectors in a second wave of translocation ( Finn et al., 2017). The T3SS-1 and SPI-1 expressed effector proteins generally help establish infection and play a role in bacterial uptake and generation of the Salmonella containing vacuole (SCV). Salmonella express two different T3SS translocons required for infection T3SS-1, encoded by Salmonella Pathogenicity Island 1 (SPI-1) along with a subset of effector proteins, and T3SS-2, encoded by Salmonella Pathogenicity Island 2 (SPI-2) along with another cohort of effector proteins (reviewed in Malik-Kale et al., 2011). T3SSs evolved from the flagellar apparatus ( Abby and Rocha, 2012) and represent a common mechanism for secretion of effector proteins ( Marlovits and Stebbins, 2010 Moest and Méresse, 2013). One way that pathogenic bacteria, such as gram negative Salmonella, deliver effectors into the host cell cytosol is through specialized secretion systems such as the type III secretion system (T3SS). These effector proteins function to modulate the host cell by commandeering signaling pathways to enable the pathogen to invade the host, evade immune responses and establish a replication-permissive environment. Members of the Enterobacteriaceae family of pathogenic bacteria, which includes Salmonella, as well as Escherichia, Yersinia, Shigella, Enterobacter, and Citrobacter express specialized virulence proteins known as effectors, which are secreted into the host during the infection process. Pathogenic bacteria have evolved to survive and proliferate inside of host cells despite an adverse environment driven by host defense mechanisms. It will describe how different approaches have revealed mechanistic details for effectors in manipulating host cellular processes including: the dynamics of effector translocation into host cells, cytoskeleton reorganization, membrane trafficking, gene regulation, and autophagy. This review will highlight the techniques applied to study Salmonella effector proteins during infection. Recent techniques for studying infection using single cell and animal models have illuminated the contribution of individual effector proteins in infection. A number of diverse and innovative approaches have been used to identify and characterize the role of effector proteins during infection. Salmonella virulence factors include a suite of effector proteins that remodel the host cell to facilitate bacterial internalization, replication, and evasion of host immune surveillance. Intracellular bacterial pathogens like Salmonella enterica use secretion systems, such as the Type III Secretion System, to deliver virulence factors into host cells in order to invade and colonize these cells. Department of Chemistry and Biochemistry, BioFrontiers Institute, University of Colorado Boulder, Boulder, CO, United States.
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