DIFFERENTIAL AND ANTAGONISTIC EFFECTS OF V-JUN AND C-JUN

We compared the ability of cellular and viral Jun (c-Jun and v-Jun) to transactivate target genes, c-Jun and v-Jun bind specifically to 12-O -tetradecanoylphorbol-13 -acetate responsive elements [TREs, also call ed activator protein 1 (AP-1) motifs], However, whereas c-Jun activate s TRE-controlled promoters, v-Jun represses them, Cotransfection of th e two Jun proteins reduces c-jun-dependent transactivation. The expres sion of the endogenous c-jun gene, regulated through a promoter-proxim al AP-1-binding site, is repressed in v-Jun-transformed chicken embryo fibroblasts. It is suggested that an M(r) 18,000 v-jun peptide promin ent in v-Jun-transformed cells acts as a transdominant-negative regula tor of AP-1 activity and of c-jun expression, In contrast to the resul ts with TRE sites, both v-Jun and c-Jun activate transcription through the human T-cell leukemia virus type I 21-bp repeat which contains a sequence homologous to the cyclic AMP responsive element, However, ful l-length Jun proteins bind to this site only with low affinity, and bi nding of the truncated v-Jun was barely detectable, These observations show that the oncogenic viral form of Jun differs from the cellular v ersion in promoter preference and on certain promoters acts as an anta gonist to c-Jun.