ABSTRACT
The occurrence of Ap4 A in rat liver was evidenced as early as 1969; the first reports suggesting a physiological role for diadenosine tetraphosphate came out in the mid-1970s. The absence of important variations in Ap4N concentrations during the cell cycle do not seem specific to eukaryotes, since Plateau et al. reported that the pools of Ap4N and Ap, N also remained constant in synchronized exponentially growing E. coli. It was also shown that anoxia as well as the release from anoxia can elicit a heat shock response in eukaryotes. Acidosis was also proposed to play a role in the induction of stress proteins. Treatment of prokaryotic or eukaryotic cells with ethanol often leads to the synthesis of heat shock proteins. The initial experiments of Baker and Jacobson using UV-irradiated cultured mammalian cells did not reveal any variation of the adenyl dinucleotide pool.
