9 Translational Control during Heat Shock

Abstract

Heat shock or heat stress, i.e., raising the temperature of cells or organisms 5–10°C above their normal growth temperature, is the principal stress system from which most of our understanding of stress-induced translational control has emerged. There are two principal events comprising translational control during heat shock: (1) a general repression of the translation of non-heat shock protein messenger RNAs (referred to here as normal mRNAs) and (2) the preferential translation of a small class of mRNAs, the heat shock protein (HSP) mRNAs. Current knowledge about the molecular basis for each is reviewed in this chapter. Substantial progress has been made in recent years, and there is reason for optimism that where uncertainty remains, molecular details will be forthcoming shortly.

A consequence of heat-shock-induced translational reprogramming is the production of massive amounts of the heat shock proteins. These enable cells to survive what would otherwise be lethal heat shock and greatly accelerate recovery of normal cell function following heat shock. This process, termed acquired thermotolerance, has been extensively reviewed elsewhere (Parsell and Lindquist 1993). At the translational level, heat shock proteins are proposed to counteract the repressive influences of heat shock, resulting in less inhibition during heat shock and a more rapid restoration of normal protein synthesis rate after heat shock. This process, termed translational thermotolerance, which is a subset of acquired thermotolerance, is described in more detail below.

The preferential translation of HSP mRNAs provides a mechanism for the rapid, massive accumulation of these beneficial proteins under adverse...