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Background  Toxin-antitoxin (TA) systems, abundant in prokaryotes, are composed of a toxin gene and its cognate antitoxin. Several toxins are implied to affect the physiological state and stress tolerance of bacteria in a population. We previously identified a chromosomally encoded  hok - sok  type I TA system in  Erwinia amylovora , the causative agent of fire blight disease on pome fruit trees. A high-level induction of the  hok  gene was lethal to  E. amylovora  cells through unknown mechanisms. The molecular targets or regulatory roles of Hok were unknown.    Results  Here, we examined the physiological and transcriptomic changes of  Erwinia amylovora  cells expressing  hok  at subtoxic levels that were confirmed to confer no cell death, and at toxic levels that resulted in killing of cells. In both conditions,  hok  caused membrane rupture and collapse of the proton motive force in a subpopulation of  E. amylovora  cells. We demonstrated that induction of  hok  resulted in upregulation of ATP biosynthesis genes, and caused leakage of ATP from cells only at toxic levels. We showed that overexpression of the phage shock protein gene  pspA  largely reversed the cell death phenotype caused by high levels of  hok  induction. We also showed that induction of  hok  at a subtoxic level rendered a greater proportion of stationary phase  E. amylovora  cells tolerant to the antibiotic streptomycin.    Conclusions  We characterized the molecular mechanism of toxicity by high-level of  hok  induction and demonstrated that low-level expression of  hok  primes the stress responses of  E. amylovora  against further membrane and antibiotic stressors.    Supplementary Information  The online version contains supplementary material available at 10.1186/s12864-021-07376-w.

Activation of metabolic and stress responses during subtoxic expression of the type I toxin hok in Erwinia amylovora