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J. Biol. Chem., Vol. 281, Issue 51, 39370-39379, December 22, 2006

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Myomaxin Is a Novel Transcriptional Target of MEF2A That Encodes a Xin-related -Actinin-interacting Protein^*

From the Department of Biology, Program in Cell and Molecular Biology, Boston University, Boston, Massachusetts 02215

The physiological targets regulated by MEF2 in striated muscle are not completely known. Several recent studies have identified novel downstream target genes and shed light on the global transcriptional network regulated by MEF2 in muscle. In our continuing effort to identify novel, downstream pathways controlled by MEF2, we have used mef2a knock-out mice to find those genes dependent on MEF2A transcriptional activity. Here, we describe the characterization of a direct, downstream target gene for the MEF2A transcription factor encoding a large, muscle-specific protein that localizes to the Z-disc/costameric region in striated muscle. This gene, called myomaxin, was identified as a gene markedly down-regulated in MEF2A knock-out hearts. Myomaxin is the mouse ortholog of a partial human cDNA of unknown function named cardiomyopathy associated gene 3 (CMYA3). Myomaxin is expressed as a single, large transcript of 11 kilobases in adult heart and skeletal muscle with an open reading frame of 3,283 amino acids. The protein encoded by the myomaxin gene is related to the actin-binding protein Xin and interacts with the sarcomeric Z-disc protein, -actinin-2. Our findings demonstrate that Myomaxin functions directly downstream of MEF2A at the peripheral Z-disc complex in striated muscle potentially playing a role in regulating cytoarchitectural integrity.

Received for publication, April 5, 2006 , and in revised form, October 5, 2006.

The nucleotide sequence(s) reported in this paper has been submitted to the GenBank^TM /EBI Data Bank with accession number EF122140 [GenBank] .

^* This work was supported by NHLBI, National Institutes of Health, Public Health Service Grant HL 73304 (to F. N.), a Clare Boothe Luce Fellowship (to S. M.), and Northeast Summer Student Research Fellowships from the American Heart Association (to H.-T. H. and M. M.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ To whom correspondence should be addressed: Dept. of Biology, Boston University, 24 Cummington St., Boston, MA 02215. Tel.: 617-353-2469; Fax: 617-353-6340; E-mail: fnaya{at}bu.edu.

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