ABSTRACT
The response of cells to a sudden shift to an elevated temperature that is not lethal leads to the rapid induction of substantially increased thermotolerance. This heat shock response is a transient process and is induced most strongly by temperature shift to the maximum growth temperature or just above it, and by the extent of the shift: the greater the temperature difference the higher the response (Kirk and Piper, 1991). Coote et al., (1991) have shown that thermotolerance is most rapidly induced by temperatures up to 45°C, which is beyond that at which protein synthesis can be detected by pulse-labelling. The induction of thermotolerance is not, however, solely brought about by temperature increase. A wide range of conditions or treatments, including ethanol at concentrations above about 4% (v/v), antibiotics inducing aberrant protein synthesis (Grant et al., 1989) or inhibiting transcription (Adams and Goss, 1991), protease inhibitors (Gropper and Rensing, 1993) or even sphaeroplasting (Piper et al., 1994) can activate the heat shock response.
