Regulation of heat-shock response in bacteria.

Abstract

Stress response in bacteria is essential for effective adaptation to changes in the environment, as well as to the changes in the physiological state of the bacterial culture itself. This response is mediated by global regulatory mechanisms affecting several pathways. It now appears that these regulatory mechanisms operate by transcriptional control, translational control, and proteolysis. One example to be discussed extensively is the heat-shock response. In Escherichia coli, where it has been studied initially and most extensively, the expression of the heat-shock operon is transcriptionally controlled by the employment of the heat-shock transcription factor sigma 32, that recognizes specific heat-shock promoters. Later studies indicated that in most bacteria the control of the major heat-shock genes is much more complicated, and involves additional--or alternative--control channels. These regulatory elements will be reviewed looking at the groE and dnaK operons. These operons, coding for the bacterial equivalent of Hsp10+60 and Hsp70, respectively, contain in many bacteria a conserved regulatory inverted repeat (IR = CIRCE), and are transcribed either by the vegetative sigma factor--sigma 70--or by a sigma 32-like factor. The IR functions at the DNA level as a repressor binding site and also controls the half life of the transcript. In addition, in Agrobacterium tumefaciens there also exists a system for mRNA processing that involves a temperature-controlled cleavage of the groE transcript.