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Vol. 59, Issue 5, 1225-1234, May 2001
1C/A-Adrenergic
Receptor Gene and Analysis of an 1C Promoter in Cardiac Myocytes:
Role of an MCAT Element That Binds Transcriptional Enhancer Factor-1
(TEF-1)
Cardiology Division and Research Service, Veterans Affairs Medical
Center, San Francisco, California; and the Cardiovascular Research
Institute and Department of Medicine, University of California, San
Francisco, California
1-Adrenergic receptor (AR) subtypes in the heart are expressed
by myocytes but not by fibroblasts, a feature that distinguishes 1-ARs from 
-ARs. Here we studied myocyte-specific expression of
1-ARs, focusing on the subtype 1C (also called 1A), a subtype implicated in cardiac hypertrophic signaling in rat models. We first
cloned the mouse 1C-AR gene, which consisted of two exons with an 18 kb intron, similar to the 1B-AR gene. The receptor coding sequence
was >90% homologous to that of rat and human. 1C-AR transcription
in mouse heart was initiated from a single Inr consensus sequence at
588 from the ATG; this and a putative polyadenylation sequence 8.5 kb
3' could account for the predominant 11 kb 1C mRNA in mouse heart. A
5'-nontranscribed fragment of 4.4 kb was active as a promoter in
cardiac myocytes but not in fibroblasts. Promoter activity in myocytes
required a single muscle CAT (MCAT) element, and this MCAT bound in
vitro to recombinant and endogenous transcriptional enhancer
factor-1. Thus, 1C-AR transcription in cardiac myocytes
shares MCAT dependence with other cardiac-specific genes, including the
- and -myosin heavy chains, skeletal -actin, and brain
natriuretic peptide. However, the mouse 1C gene was not transcribed
in the neonatal heart and was not activated by 1-AR and other
hypertrophic agonists in rat myocytes, and thus differed from other
MCAT-dependent genes and the rat 1C gene.
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