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Volume 271, Number 49, Issue of December 6, 1996 pp. 31688-31694
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.

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The Myogenic Regulatory Factor MRF4 Represses the Cardiac -Actin Promoter through a Negative-acting N-terminal Protein Domain

(Received for publication, June 25, 1996, and in revised form, August 20, 1996)

From the Department of Cell Biology, Baylor College of Medicine, Houston, Texas 77030 and the ^¶ Hamon Center for Basic Cancer Research, University of Texas Southwestern Medical Center, Dallas, Texas 75235

Cardiac -actin is activated early during the development of embryonic skeletal muscle and cardiac myocytes. The gene product remains highly expressed in adult striated cardiac muscle yet is dramatically reduced in skeletal muscle. Activation and repression of cardiac -actin gene activity in developing skeletal muscle correlates with changes in the relative content of the four myogenic regulatory factors. Cardiac -actin promoter activity, assessed in primary chick myogenic cultures, was activated by endogenous myogenic regulatory factors but was inhibited in the presence of co-expressed MRF4. By exchanging N- and C-terminal domains of MRF4 and MyoD, the N terminus of MRF4 was identified as the mediator of repressive activity, revealing a novel negative regulatory role for MRF4. The relative ratios of myogenic regulatory factors may have fundamental roles in selecting specific muscle genes for activation and/or repression.

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