Abstract
Shigella spp. are one of the leading causes of infectious diarrheal diseases. They are Escherichia coli pathovars that are characterized by the harboring of a large plasmid that encodes most virulence genes, including a type III secretion system (T3SS). The archetypal element of the T3SS is the injectisome, a syringe-like nanomachine composed of approximately 20 proteins, spanning both bacterial membranes and the cell wall, and topped with a needle. Upon contact of the tip of the needle with the plasma membrane, the injectisome secretes its protein substrates into host cells. Some of these substrates act as translocators or effectors whose functions are key to the invasion of the cytosol and the cell-to-cell spread characterizing the lifestyle of Shigella spp. Here, we review the structure, assembly, function, and methods to measure the activity of the injectisome with a focus on Shigella, but complemented with data from other T3SS if required. We also present the regulatory cascade that controls the expression of T3SS genes in Shigella. Finally, we describe the function of translocators and effectors during cell-to-cell spread, particularly during escape from the vacuole, a key element of Shigella’s pathogenesis that has yet to reveal all of its secrets.
Highlights
Shigella spp. are important human pathogens infecting the large intestine and responsible for hundreds of millions of infections every year [1,2]. They mainly differ from commensal Escherichia coli by the presence of a large virulence plasmid (VP) that encodes the various components of the Shigella type III secretion system (T3SS)
The first three players coordinate the transcriptional response to the rise of temperature occurring upon Shigella’s transition from an external environment to its host. The interaction between these factors and DNA culminates with the production of VirB, which activates the expression of most T3SS genes, ensuring that the T3SA is assembled in the Shigella membrane only when it is inside its host
This study proposed that IcsB protected IcsA from direct recognition by the autophagy core component ATG5 to prevent the capture of Shigella in autophagosomes
Summary
Shigella spp. are important human pathogens infecting the large intestine and responsible for hundreds of millions of infections every year [1,2]. They mainly differ from commensal Escherichia coli by the presence of a large virulence plasmid (VP) that encodes the various components of the Shigella type III secretion system (T3SS). The effectors allow the invasion of the cytosol of epithelial cells by Shigella This entry process is akin to phagocytosis. We discuss the structure and function of the T3SA, the regulation of the expression of T3SS genes, and recent progress in our understanding of the role of T3SA effectors in vacuole escape
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