Bacteria are separated from their environment by a complex multi-layered envelope. Pathogenic bacteria, in particular gram-negative bacteria, are a major group among the pathogens associated with diseases in aquatic organisms and have evolved multiple features to influence their hosts and defend themselves against attackers. This increased production has been in part achieved by increasing the intensity of fish farming, which has led to an increase in the occurrence of infectious diseases, which represent a major limiting factor in aquaculture. Aquaculture has become the fastest growing animal food production sector and it is expected to almost double to reach 93.2 million tons in the next decade.
The demand for fish products has been increasing worldwide for multiple decades now, and with the output of fisheries largely stagnant, this demand has been mostly answered through the growth of aquaculture, particularly in developing countries. In the present review, we summarise what is known of the T3SS, with a special focus on aquatic pathogens and suggest some possible avenues for research including the potential to target the T3SS for the development of new anti-virulence drugs.
This is also the case in aquatic bacterial pathogens where the T3SS can often play a central role in the establishment of disease, although it remains understudied in several species of important fish pathogens, notably in Yersinia ruckeri. The T3SS can remodel the cytoskeleton integrity to promote intracellular invasion, as well as silence specific eukaryotic cell signals, notably to hinder or elude the immune response and cause apoptosis. While the structure of the T3SS is somewhat conserved and well described, effector proteins are much more diverse and specific for each pathogen. The T3SS constitutes a needle-like apparatus that the bacterium uses to inject a diverse set of effector proteins directly into the cytoplasm of the host cells where they can hamper the host cellular machinery for a variety of purposes. Additional analysis demonstrated that YopP and YspH secretion was resto.Gram-negative bacteria are known to subvert eukaryotic cell physiological mechanisms using a wide array of virulence factors, among which the type three-secretion system (T3SS) is often one of the most important. These results indicate YspG, YspH, and YspJ are actually YopN, YopP, and YopE. Furthermore, mutations in yopN, yopP, and yopE specifically blocked YopN, YopP, and YopE secretion by the Ysc TTSS and YspG, YspH, and YspJ secretion by the Ysa TTSS. Immunoblot analysis demonstrated that antibodies directed against YopN, YopP, and YopE recognized YspG, YspH, and YspJ. enterocolitica indicated that YspG, YspH, and YspJ have apparent molecular masses similar to those of YopN, YopP, and YopE, respectively. A comparison of Ysps with Yop effectors secreted by Y. This indicated that YspG, YspH, and YspJ are encoded by genes located on pYVe8081 and that they may correspond to Yops. Furthermore, mutations that blocked the function of the Ysc TTSS did not affect YspG, YspH, and YspJ production. In this study, secretion of YspG, YspH, and YspJ by the Ysa TTSS was shown to require pYVe8081. The Ysc TTSS and the Yop effector proteins it exports are encoded by genes located on plasmid pYVe8081. The Ysa TTSS is encoded by a set of genes located on the chromosome and exports Ysp proteins.
Yersinia enterocolitica O:8 has two contact-dependent type III secretion systems (TTSSs).
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