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(Received for publication, June 30,
1994; and in revised form, October 21, 1994) Induction of the fetal isogenes skeletal
Volume 270,
Number 1,
Issue of January 6, 1995 pp. 410-417
©1995 by The American Society for Biochemistry and Molecular Biology, Inc.
-Adrenergic
Induction of the Skeletal
-Actin Promoter during Cardiac Myocyte
Hypertrophy
TRANSCRIPTIONAL ENHANCER FACTOR-1 AND PROTEIN KINASE C AS CONSERVED
TRANSDUCERS OF THE FETAL PROGRAM IN CARDIAC GROWTH
-actin (skACT) and
-myosin heavy chain (-MHC) is characteristic of cardiac
growth in many models, suggesting a conserved signaling pathway.
However, divergent regulation has also been observed. -Protein
kinase C (PKC) and transcriptional enhancer factor-1 (TEF-1) are
involved in induction of -MHC in
-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 -adrenergic
stimulation and co-transfection of activated -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
-MHC promoters both require a TEF-1 binding site for activation by
-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.
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