Introduction

Abstract

The response to environmental and physiological stress includes a highly ordered set of events that is often represented by rapid changes in gene expression followed by the synthesis of proteins involved in adaptation to the stress. Two examples presented in this section include the SOS response to DNA damaged the heat shock response to protein damage. The genes involved in the SOS response are under the regulation of recA and lexA gene products of which lexA acts to repress the transcription of genes involved in repair mechanisms. A consequence of these events is the reduced fidelity of DNA replication to allow error-prone synthesis, the accumulation of mutations and cell survival. The SOS response provides unique insights into cell survival mechanisms at the level of protection of the genome. By comparison, the heat shock response in prokaryotes utilizes the s³² and s^E proteins as positive activators of genes encoding heat shock proteins and molecular chaperones. The mechanism by which s³² levels increase following heat shock involves a novel post-translational process in which there is increased translation of s³² RNA and stabilization of s³² which involves interactions with dnaK, dnaJ, and grpE in a complex autoregulatory loop. In eukaryotes, the heat shock transcriptional response is mediated by members of the heat shock factor (HSF) family. The process by which the HSFs are regulated in response to stress and negatively regulated under conditions of normal cell growth reveals an understanding of the mechanisms by which the eukaryotic cell detects stress. Among the other well studied events of the stressed cell are changes in protein folding/protein unfolding and on protein modification such as phos-phorylation. These “inducible” events may be integrated to diminish some of the deleterious effects of prolonged stress and as a means of signaling components of the replication, transcription, and translation machinery. Together, these examples provide a representative presentation of inducible stress response.