17 Translational Control during Heat Shock

Abstract

HEAT SHOCK RESPONSE INVOLVES TRANSLATIONAL CONTROL
Heat shock is a thermally induced stress response in cells or organisms at 5–10°C above their normal physiological temperature (for review, see Lindquist 1986). Cells respond to heat in a conserved manner to protect against hyperthermic lethality and to accelerate recovery following heat stress. The heat shock response in most organisms and cells includes inhibition of protein synthesis above a characteristic threshold temperature, with the exclusive translation of heat shock protein mRNAs (for review, see Panniers 1994). The extent of inhibition of non-heat shock (“normal”) mRNA translation increases with the severity of heat shock. The higher the temperature and the longer the exposure of cells, the greater the inhibition of normal mRNA translation and the longer the interval for recovery of protein synthesis following heat shock (for review, see Duncan 1996). Following heat shock, cells can acquire translational thermotolerance, in which they possess a more rapid ability to recover normal protein synthesis following heat stress, and sometimes a greater ability to maintain translation during subsequent rounds of heat shock (Mizzen and Welch 1988; Beck and De Maio 1994). In most cells (except yeast), mRNAs are not degraded or modified during heat shock, and they can be translated in vitro (Kruger and Benecke 1981). The translational apparatus is therefore altered to prevent translation of normal mRNAs. The block in normal mRNA translation during heat shock involves disassembly of polysomes and inhibition of initiation (for review, see Panniers 1994; Duncan 1996). In Drosophila cells there...