UV‐induced activation of AP‐1 involves obligatory extranuclear steps including Raf‐1 kinase.

Signals elicited from different primary sites merge prior to or at the level of activation of Raf‐1 kinase, indicating obligatory involvement of identical components in cytoplasmic signal transduction.

Abstract

Irradiation of cells with ultraviolet light (UV) leads to modifications of c-Jun resembling those elicited by phorbol esters or oncogenes, and to enhanced transcription of AP-1-dependent genes. The UV-induced signal also triggers activation of Raf-1 and MAP-2 kinases. A dominant-negative Raf-1 kinase mutant strongly interferes with both phorbol ester and UV-induced AP-1 activation, indicating obligatory involvement of identical components in cytoplasmic signal transduction. Thus, from a presumably nuclear site of energy absorption, a signal needs to be transmitted to the cytoplasm in order to achieve activation of a nuclear transcription factor. Further, signals elicited from different primary sites merge prior to or at the level of activation of Raf-1 kinase.