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

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