Abstract
As part of the cellular response to sublethal heat stress there is a rapid and coordinated increase in the expression of a group of proteins, the heat shock proteins (HSPs), or stress proteins (see Burdon 1986, 1988; Lindquist 1986). It is now clear that at least some of these stress proteins are essential for the survival of cells confronted with temperature and other stresses. In addition to elevated temperatures, a variety of other treatments will elicit the increased production of the HSPs. These include certain heavy metals, high levels of ethanol and amino acid analogues. Because of the possibility that these alternative inducers, like heat, could create abnormal protein structures within the cell, it is believed that the intracellular accumulation of abnormal proteins may be an important element in mechanisms leading to HSP induction (Munro and Pelham 1985; Anathan et al. 1986).
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