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Type III secretion systems (T3SS) are probably the most impressive of the secretion systems (see Galan and Waksman, Suggested Reading). They form a syringe-like structure composed of about 20 proteins, which takes up virulence proteins called effectors from the cytoplasm of the bacterium and injects them directly through both membranes into a eukaryotic cell (Figure 2.39). For this reason, they are sometimes called injectisomes. They exist in many Gram-negative animal pathogens, including Salmonella and Yersinia, but are also found in many plant pathogens, including Erwinia and Xanthomonas. One striking feature of T3SS is how similar they are in both animal and plant pathogens. Where they differ is in the protuberance, called the needle, that penetrates the eukaryotic cell to allow injection through the wall into the host cell cytoplasm. This difference is expected, because animal and plant cells are surrounded by very different cell surfaces.

T3SS are usually encoded on pathogenicity islands (see chapter 12), and their genes are induced only when the bacterium encounters its host or if they are cultivated under conditions that are designed to mimic the host. The effector proteins they inject are also encoded by the same DNA element, and their genes are turned on at the same time. The part of the injectisome that traverses the outer membrane is composed of a secretin protein related to those of the T2SS. It also forms a β-barrel composed of about a dozen secretin subunits. Like the secretins of the T2SS, these might require normal bacterial lipoproteins, as well as other components of the secretion machinery, to assemble the channel in the membrane.

Effector proteins to be secreted by at least some T3SS contain a short sequence located on the N terminus of the protein; unlike the cleavable signal sequences used by the Sec and Tat systems, this signal is not cleaved off when the protein is secreted. Many of the effector proteins injected into eukaryotic cells are involved in subverting the host defenses against infection by bacteria. This can be illustrated by Yersinia pestis, the bacterium that causes bubonic plague and in which T3SS were first discovered. In amimals, one of the first lines of defense against infecting bacteria is the macrophages, phagocytic white blood cells that engulf invading bacteria and destroy them by emitting a burst of oxidizing compounds. However, when a macrophage binds to a Yersinia cell, the bacterium injects effectors called Yop proteins into the macrophage cell before it can be engulfed. Once in the eukaryotic cell, these effectors disarm the cell by interfering with its signaling systems and thus preventing the macrophage from engulfing the bacterium. For example, one of the Yop proteins is a tyrosine phosphatase, which removes phosphates from proteins in a signal transduction system in the macrophage, blocking the signal to take up the bacterium and preventing the burst of oxidizing compounds. Some T3SS even inject proteins that provide receptors on the cell surface to which the bacterium can adsorb in order to enter the eukaryotic cell.