The myogenic regulatory factor MRF4 represses the cardiac alpha-actin promoter through a negative-acting N-terminal protein domain.

The Journal of Biological Chemistry
J B MossRobert J Schwartz

Abstract

Cardiac alpha-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 alpha-actin gene activity in developing skeletal muscle correlates with changes in the relative content of the four myogenic regulatory factors. Cardiac alpha-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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Citations

Feb 27, 2010·European Journal of Applied Physiology·Micah J DrummondAllen C Parcell
Oct 23, 2004·Developmental Dynamics : an Official Publication of the American Association of Anatomists·Christophe ChanoineFrédéric Charbonnier
Aug 4, 2016·Nature Communications·Irene MorettiStefano Schiaffino
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Jul 18, 2009·Journal of the American College of Cardiology·Mousumi MoulikJeffrey A Towbin

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