Temperature-dependent expression of virulence genes in fish-pathogenic bacteria.
Bottom Line: A key factor in this expression is temperature.This is an interesting issue and progress needs to be made in order to diminish the economic losses caused by these diseases.The intention of this review is, for the first time, to compile the scattered results existing in the field in order to lay the groundwork for future research.
Virulence gene expression in pathogenic bacteria is modulated by environmental parameters. A key factor in this expression is temperature. Its effect on virulence gene expression in bacteria infecting warm-blooded hosts is well documented. Transcription of virulence genes in these bacteria is induced upon a shift from low environmental to a higher host temperature (37°C). Interestingly, host temperatures usually correspond to the optimum for growth of these pathogenic bacteria. On the contrary, in ectothermic hosts such as fish, molluscs, and amphibians, infection processes generally occur at a temperature lower than that for the optimal growth of the bacteria. Therefore, regulation of virulence gene expression in response to temperature shift has to be modulated in a different way to that which is found in bacteria infecting warm-blooded hosts. The current understanding of virulence gene expression and its regulation in response to temperature in fish-pathogenic bacteria is limited, but constant extension of our knowledge base is essential to enable a rational approach to the problem of the bacterial fish diseases affecting the aquaculture industry. This is an interesting issue and progress needs to be made in order to diminish the economic losses caused by these diseases. The intention of this review is, for the first time, to compile the scattered results existing in the field in order to lay the groundwork for future research. This article is an overview of those relevant virulence genes that are expressed at temperatures lower than that for optimal bacterial growth in different fish-pathogenic bacteria as well as the principal mechanisms that could be involved in their regulation.
No MeSH data available.
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Mentions: Temperature-dependent gene expression could also be mediated by means of proteins. Amongst the different regulation mechanisms in which proteins are involved, those based on repressing promoter activity at TBO by protein DNA binding and further protein-DNA disassembling at host temperatures (37°C) deserve special attention. Examples of this kind of regulation are the TlpA and HtrA proteins of S. enterica (Gal-Mor et al., 2006) and in Helicobacter pylori (Hoy et al., 2012), respectively, both involved in the virulence of these bacteria. These regulation systems are of interest, but, may not participate in virulence gene modulation in fish-pathogenic bacteria. However, it is important to consider two other mechanisms that could well be involved in virulence gene regulation at TBO: protein conformational changes that abolish DNA-binding at host temperature (37°C), stopping gene transcription, i.e., the RovA system in Yersinia species (Ellison et al., 2004; Marceau, 2005; Cathelyn et al., 2006); and the repressor/antirepressor complex MogR:GmaR regulating motility of Listeria monocytogenes (Kamp and Higgins, 2011). In both cases, gene expression takes place at TBO and it is impaired at host temperature (37°C). In Yersinia enterocolitica, RovA binds at 25°C at the 5′end of the inv gene, activating its transcription to produce invasin, a protein involved in the first steps of tissue colonization (Ellison et al., 2004; Figure 3). At 37°C a conformational RovA change prevents its binding to DNA and makes it susceptible to degradation by the Lon protease (Herbst et al., 2009), impeding gene expression (Cathelyn et al., 2006; Ellison and Miller, 2006; Figure 3). As in Yersinia, the first steps of the infection process in L. monocytogenes imply the activation of genes at temperatures below 30°C. In particular, genes related to motility are needed for bacterial entry into the host cells (O’Neil and Marquis, 2006). This flagelar motility (flaA gene) is temperature-regulated through the GmaR:MogR complex, which once bound to the upstream promoter region, enables flaA gene expression of L. monocytogenes at 30°C (Kamp and Higgins, 2011). Conformational changes in GmaR at 37°C prevent its union to MogR, which is thus able to act as a repressor of the flaA gene by itself (Shen and Higgins, 2006), blocking its expression and rendering the bacterial cells non-motile just after invasion has occurred.
No MeSH data available.