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Endocrinology, Vol 133, 1934-1940, Copyright © 1993 by Endocrine Society

ARTICLES

Protooncogene junB as a target for activin actions

M Hashimoto, D Gaddy-Kurten and W Vale
Clayton Foundation Laboratories for Peptide Biology, Salk Institute for Biological Studies, La Jolla, California 92037-1099.

Activin, a member of the transforming growth factor-beta family of peptides, is implicated in the regulation of cell growth and differentiation in a variety of biological systems. We have sought to identify immediate early genes whose altered expression may provide a common nuclear event involved in activin-regulated phenotypic changes in many cell types. In both human K562 myelogenous leukemia and rat PC12 pheochromocytoma cells, activin treatment caused transient transcription-dependent and protein synthesis-independent increases of junB messenger RNA (mRNA) within 1 h, whereas neither c-jun nor c-fos mRNA were inducible. In K562 cells, this selective junB mRNA induction was synergistically augmented by treatment with 12-O-tetradecanoyl phorbol-13-acetate but not affected by forskolin. Furthermore, in PC12 cells, the up-regulation of junB mRNA by activin was observable even after high-dose treatment with 12-O-tetradecanoyl phorbol-13-acetate for 48 h, indicating that junB mRNA expression by activin is independent of both A- and C-kinases. Our report suggests that induction of this ubiquitous gene product may be a critical event shared by a set of activin-responsive tissues.


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