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Originally published In Press as doi:10.1074/jbc.M000518200 on March 15, 2000

J. Biol. Chem., Vol. 275, Issue 28, 21453-21459, July 14, 2000
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Analysis of CMF1 Reveals a Bone Morphogenetic Protein-independent Component of the Cardiomyogenic Pathway*

Lil M. Pabón-Peña, Richard L. Goodwin, Linda J. Cise, and David BaderDagger

From the Program for Developmental Biology, Stahlman Cardiovascular Research Laboratories, Division of Cardiovascular Medicine, Vanderbilt University, Nashville, Tennessee 37232-6300

Disruption of the CMF1 function in anterior mesoderm inhibits cardiac myogenesis in avian embryos. In the present study, we show that CMF1 is a member of an emerging family of proteins that includes centromeric protein-F, mitosin, and LEK1. These proteins are characterized by their large size (350 kDa), dynamic subcellular distribution, and potential functions in cell division and differentiation. The current data suggest that CMF1 is a unique member of this family by virtue of its restricted protein expression and variant subcellular distribution. Immunochemical analysis demonstrates that CMF1 protein is expressed in cardiogenic cells prior to the activation of cardiac structural gene products. In addition, we show that expression of CMF1 is not dependent on the bone morphogenetic protein (BMP) signaling pathway during development. Still, CMF1 cannot direct cardiomyogenesis in the absence of such factors as NKX-2.5. Taken with our previous data, this study suggests that CMF1 is a BMP-independent component of the cardiomyogenic pathway.


* This work was supported by National Institutes of Health (NIH) Grants HL37617 (to D. B.) and HL09916 (to R. L. G.) and NIH Training Grant HL07723 (to L. P-P.). The Vanderbilt University Medical College Cell Imaging Resource is supported by National Institutes of Health Grants CA68485 and DK20593.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Dagger To whom correspondence should be addressed: Stahlman Cardiovascular Research Labs., Div. of Cardiovascular Medicine, Vanderbilt University, Rm. 338, MRB II, 2220 Pierce Ave., Nashville, TN 37232-6300. Tel.: 615-936-1976; Fax: 615-936-3527; E-mail: david.bader@mcmail.vanderbilt.edu.


Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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