Abstract
The hok/sok locus is renowned for its plasmid stabilization effect via post-segregational killing of plasmid-free daughter cells. However, the function(s) of the chromosome-encoded loci, which are more abundant in pathogenic strains of a broad range of enteric bacteria, are yet to be understood. Also, the frequent occurrence of this toxin/antitoxin addiction system in multi-drug resistance plasmids suggests additional roles. In this study, the effects of the hok/sok locus on the growth of bacteria in stressful growth-limiting conditions such as high temperature and antibiotic burden were investigated using hok/sok plasmids. The results showed that the hok/sok locus prolonged the lag phase of host cell cultures, thereby enabling the cells to adapt, respond to the stress and eventually thrive in these growth-limiting conditions by increasing the growth rate at exponential phase. The hok/sok locus also enhanced the survival and growth of cells in low cell density cultures irrespective of unfavourable growth conditions, and may complement existing or defective SOS mechanism. In addition to the plasmid stabilization function, these effects would enhance the ability of pathogenic bacteria to establish infections and propagate the antibiotic resistance elements carried on these plasmids, thereby contributing to the virulence of such bacteria.
Highlights
The hok/sok locus is a well established type 2 toxin/antitoxin system which was originally discovered due to its stabilizing activity on the inheritance of plasmid R1 [1]
The plasmid stabilization function of the hok/sok locus was found to be affected by factors such as temperature, growth rate and dilution rates in a study in which a temperature sensitive plasmid was used without antibiotic selection [21]
Bearing in mind that the R1 plasmid in which the hok/sok locus occurs naturally is associated with multi-drug resistance, these results strongly indicate that the hok/sok locus contributes to antibiotic resistance
Summary
The hok/sok locus is a well established type 2 toxin/antitoxin system which was originally discovered due to its stabilizing activity on the inheritance of plasmid R1 [1]. In daughter cells that have lost the plasmid, the acquired Sok RNA are more rapidly degraded than the hok mRNA, thereby releasing the more stable hok mRNA for translation and subsequent cell death by the toxin produced. In this way, the hok/sok locus efficiently ensures that all surviving daughter cells inherit the plasmid by killing plasmid-free daughter cells, thereby playing a major role in plasmid maintenance and stability [4]. Chromosomally-encoded hok/sok loci are more abundant in pathogenic strains of E. coli [10]
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