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M-CAT, CArG, and Sp1 Elements Are Required for -Adrenergic Induction of the Skeletal -Actin Promoter during Cardiac Myocyte Hypertrophy

Induction of the fetal isogenes skeletal α-actin (skACT) and β-myosin heavy chain (β-MHC) is characteristic of cardiac growth in many models, suggesting a conserved signaling pathway. However, divergent regulation has also been observed. β-Protein kinase C (PKC) and transcriptional enhancer factor-1 (TEF-1) are involved in induction of β-MHC in α1-adrenergic-stimulated hypertrophy of cultured cardiac myocytes (Kariya, K., Farrance, I. K. G., and Simpson, P. C.(1993) J. Biol. Chem. 268, 26658-26662; Kariya, K., Karns, L. R., and Simpson, P. C.(1994) J. Biol. Chem. 269, 3775-3782). In the present study, we asked whether the skACT promoter used the same mechanism. A mouse skACT promoter fragment (−113/−46) was induced by both α1-adrenergic stimulation and co-transfection of activated β-PKC, and contained three required DNA sequence elements: M-CAT, CArG, and Sp1. The skACT M-CAT element bound TEF-1 in cardiac myocytes. Thus the skACT and β-MHC promoters both require a TEF-1 binding site for activation by α1-adrenergic stimulation, but differ in that skACT also requires a CArG box. These results provide a potential molecular basis for divergent regulation of the fetal program, and also imply that PKC and TEF-1 are conserved transducers for this program during cardiac growth.