The Jun oncoprotein is the major component of the transcriptional complex AP-1, which is involved in several cell functions. Constitutive activation of AP-1 is required for cell transformation, and also occurs in distinct human tumor cells. Jun is able to dimerize with different partners including Fos family members and ATF proteins providing AP-1 with high flexibility in gene regulation and functions. Particularly, by using mutants selective for Fos proteins or ATF2-like proteins, it has been demonstrated that v-Jun-induced transformation phenotype consists of, at least, two distinct, complementing genetic programs.
It has been long known that transformation of myogenic cells by v-Jun, as well as by activated c-Jun, prevents terminal differentiation. In order to better dissect the transformation activity exerted by Jun in myogenic cells, C2C12 cells were infected with retroviral vectors expressing v-Jun mutants selective for Fos proteins or ATF2-like proteins. The analysis of the different cell population revealed opposite phenotypes induced by the different mutants. Data supporting the major role of v-Jun:ATF dimer in the inhibition of terminal differentiation will be presented
