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Molecular and Cellular Biology, January 2007, p. 518-525, Vol. 27, No. 2
0270-7306/07/$08.00+0     doi:10.1128/MCB.01415-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Regulation of HDAC9 Gene Expression by MEF2 Establishes a Negative-Feedback Loop in the Transcriptional Circuitry of Muscle Differentiation{triangledown}

Michael Haberland, Michael A. Arnold, John McAnally, Dillon Phan, Yuri Kim, and Eric N. Olson*

Department of Molecular Biology, University of Texas Southwestern Medical Center, 6000 Harry Hines Boulevard, Dallas, Texas 75390

Received 1 August 2006/ Returned for modification 29 August 2006/ Accepted 27 October 2006

Skeletal muscle development is controlled by the myocyte enhancer factor (MEF2) and myogenic basic helix-loop-helix (bHLH) families of transcription factors, which associate and synergistically activate muscle gene expression. Muscle differentiation is further reinforced by positive-feedback loops in which myogenic bHLH proteins activate their own expression and the expression of MEF2, while MEF2 stimulates expression of myogenic bHLH genes and the Mef2c gene. Here we describe a myogenic negative-feedback loop that consists of MEF2 proteins and the transcriptional repressor histone deacetylase 9 (HDAC9). We show that the HDAC9 gene is a direct transcriptional target of MEF2 in vitro and in vivo. HDAC9 can associate with MEF2 proteins and suppress their transcriptional activity. The transcriptional repressor HDAC9 thus forms a negative-feedback loop in the transcriptional circuitry of muscle differentiation.

* Corresponding author. Mailing address: Department of Molecular Biology, University of Texas Southwestern Medical Center, 6000 Harry Hines Boulevard, Dallas, TX 75390. Phone: (214) 648-1187. Fax: (214) 648-1196. E-mail: eric.olson{at}utsouthwestern.edu.

{triangledown} Published ahead of print on 13 November 2006.

Molecular and Cellular Biology, January 2007, p. 518-525, Vol. 27, No. 2
0270-7306/07/$08.00+0     doi:10.1128/MCB.01415-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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