TRANSCRIPTIONAL ENHANCER FACTOR-I IN CARDIAC MYOCYTES INTERACTS WITH AN ALPHA(1)-ADRENERGIC-PROTEIN AND BETA-PROTEIN KINASE-C-INDUCIBLE ELEMENT IN THE RAT BETA-MYOSIN HEAVY-CHAIN PROMOTER

In cultured rat cardiac myocytes, a 20-base pair sequence (-215/-196) of the rat beta-myosin heavy chain (MHC) promoter mediates induction b y both alpha1-adrenergic stimulation and a constitutively activated be ta-protein kinase C (PKC), and binds cardiac myocyte nuclear factor(s) through an ''enhancer core'' element (5'-TGTGGTATG-3') (Kariya, K, Ka rns, L. R., and Simpson, P. C. (1994) J. Biol. Chem. 269, in press). H ere, we report identification of this enhancer core binding factor as the rat homologue of transcriptional enhancer factor-1 (TEF-1), a huma n transcription factor for viral enhancers. In gel mobility shift and immunoblot analyses, the myocyte factor and human TEF-1 were indisting uishable in terms of sequence recognition, mobility, and immunoreactiv ity. Furthermore, DNA binding activity for the beta-MHC enhancer core and TEF-1 immunoreactivity correlated closely. These results are the f irst to suggest a role for TEF-1 in transcriptional regulation by PKC. The data also provide direct evidence for interaction of TEF-1 with t he beta-MHC promoter, supporting a function for TEF-1 in regulation of cellular gene expression, as well as viral, and outline a pathway for alpha1-adrenergic regulation of beta-MHC gene transcription in cardia c myocytes.