ABSTRACT
Mammalian cells, when exposed to a non-lethal heat shock, can acquire a transient resistance to one or more subsequent exposures at elevated temperatures. This phenomenon has been termed thermotolerance (Gerner 1983; Gerner, et al., 1975; Henle, et al., 1978; Henle, et al., 1976). On the molecular level, heat shock activates a specific set of genes, the so-called heat shock genes, resulting in the preferential synthesis of heat shock proteins (Lindquist 1986; Lindquist, et al., 1988; Morimoto, et al., 1990).
