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.
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Mentions: RNA thermometers modulate translation efficiency of a particular mRNA in relation to temperature (Eriksson et al., 2002; Johansson and Cossart, 2003; Kortmann and Narberhaus, 2012; Han et al., 2013; Steinmann and Dersch, 2013; Grosso-Becerra et al., 2014; Weber et al., 2014). They are sequences able to form intramolecular stem-loop structures affecting the ribosomal binding site (RBS) and the translation initiation codon. In that way, at low temperature, the mRNA conformation makes the RBS site inaccessible to the ribosome. When temperature increases and, in particular, at host temperature (37°C), there is a stem-loop melting with a conformational change at the mRNA 5′end, rendering the RBS accessible to the ribosome and making mRNA translation possible. This system depends on the high stability at low temperatures of mRNA 5′sequences involved in sequestering RBS. Therefore, it seems that this mechanism would not be appropriate for regulating virulence gene expression at TBO in fish-pathogenic bacteria. However, an RNA thermo-switch has already proved to be involved in gene regulation at TBO and it could be a system implicated in the regulation of virulence genes in fish-pathogenic bacteria. Thus, at optimal bacterial growth temperatures, the RNA forms stem-loops sequestering RBS and preventing virulence gene expression, whereas at TBO, RNA conformation changes, resulting in an accessible RBS and the initiation of translation (Kortmann and Narberhaus, 2012; Steinmann and Dersch, 2013). An example of this kind of regulation system is the cspA gene of Escherichia coli involved in the cold shock response (Yamanaka et al., 1999; Giuliodori et al., 2010). Indeed, cspA mRNA undergoes a structural rearrangement at low temperature in relation to the conformation at 37°C, resulting in more efficient translation. At 37°C the 5′end of the transcribed cspA mRNA forms a secondary structure in which RBS is occluded, whereas at 10°C, an entirely new secondary structure is formed, leaving the RBS sequence accessible to the ribosome (Giuliodori et al., 2010; Figure 2).
No MeSH data available.