An array of stress signals triggering the bacterial cellular stress response is well known in Escherichia coli and other bacteria. Heat stress is usually sensed through the misfolded outer membrane porin (OMP) precursors in the periplasm, resulting in the activation of σ(E) (encoded by rpoE), which binds to RNA polymerase to start the transcription of genes required for responding against the heat stress signal. At the elevated temperatures, σ(E) also serves as the transcription factor for σ(H) (the main heat shock sigma factor, encoded by rpoH), which is involved in the expression of several genes whose products deal with the cytoplasmic unfolded proteins. Besides, oxidative stress in form of the reactive oxygen species (ROS) that accumulate due to heat stress, has been found to give rise to viable but non-culturable (VBNC) cells at the early stationary phase, which is in turn lysed by the σ(E)-dependent process. Such lysis of the defective cells may generate nutrients for the remaining population to survive with the capacity of formation of colony forming units (CFUs). σ(H) is also known to regulate the transcription of the major heat shock proteins (HSPs) required for heat shock response (HSR) resulting in cellular survival. Present review concentrated on the cellular survival against heat stress employing the harmonized impact of σ(E) and σ(H) regulons and the HSPs as well as their inter connectivity towards the maintenance of cellular survival.
Keywords: Escherichia coli; Heat shock proteins (HSPs); Heat stress; Programmed cell death (PCD); σE; σH.