Detection of an adenovirus E1A-like activity in mammalian cells.

Abstract

The E1A gene product of adenovirus is responsible for the activation of early viral transcription during a lytic infection (Jones & Shenk, 1979; Berk et al., 1979; Nevins, 1981). We have previously proposed that the E1A gene product mediates transcriptional activation through an indirect mechanism, possibly involving the inactivation of a cellular negative acting regulatory element (Nevins, 1981). This notion has been strengthened by the findings that a heterologous activator, the herpesvirus immediate early gene product, can fully supply E1A function for the activation of the adenovirus genes (Feldman et al., 1982; Imperiale et al., 1983). Furthermore, at least one cellular gene, that encoding a 70kd heat shock protein, is activated as a result of the action of the E1A protein (Nevins, 1982; Kao & Nevins, 1983). Thus, it is quite clear that the activation process mediated by E1A is not an adenovirus-specific mechanism but rather appears to be a more general mechanism of transcriptional control. We have questioned whether or not the control mediated by the E1A gene is also a control mechanism normally operating in the cell. To attempt to define such a cellular E1A-like activity, we have studied the control of the expression of the heat shock gene during normal cell growth.KeywordsWI38 CellHeat Shock Gene70kd Heat Shock ProteinTeratocarcinoma Stem CellDibutyryl Cyclic Adenosine MonophosphateThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.