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Molecular and Cellular Biology, August 2007, p. 5910-5920, Vol. 27, No. 16
0270-7306/07/$08.00+0     doi:10.1128/MCB.01700-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Determinants of Myogenic Specificity within MyoD Are Required for Noncanonical E Box Binding{triangledown} ,{dagger}

Analeah B. Heidt, Anabel Rojas, Ian S. Harris, and Brian L. Black*

Cardiovascular Research Institute and Department of Biochemistry and Biophysics, University of California, San Francisco, San Francisco, California 94158-2517

Received 10 September 2006/ Returned for modification 27 November 2006/ Accepted 21 May 2007

The MyoD family of basic helix-loop-helix (bHLH) transcription factors has the remarkable ability to induce myogenesis in vitro and in vivo. This myogenic specificity has been mapped to two amino acids in the basic domain, an alanine and threonine, referred to as the myogenic code. These essential determinants of myogenic specificity are conserved in all MyoD family members from worms to humans, yet their function in myogenesis is unclear. Induction of the muscle transcriptional program requires that MyoD be able to locate and stably bind to sequences present in the promoter regions of critical muscle genes. Recent studies have shown that MyoD binds to noncanonical E boxes in the myogenin gene, a critical locus required for myogenesis, through interactions with resident heterodimers of the HOX-TALE transcription factors Pbx1A and Meis1. In the present study, we show that the myogenic code is required for MyoD to bind to noncanonical E boxes in the myogenin promoter and for the formation of a tetrameric complex with Pbx/Meis. We also show that these essential determinants of myogenesis are sufficient to confer noncanonical E box binding to the E12 basic domain. Thus, these data show that noncanonical E box binding correlates with myogenic potential, and we speculate that the myogenic code residues in MyoD function as myogenic determinants via their role in noncanonical E box binding and recognition.

* Corresponding author. Mailing address: Cardiovascular Research Institute, Genentech Hall, 600 16th Street, Mail Code 2240, University of California, San Francisco, San Francisco, CA 94158-2517. Phone: (415) 502-7628. Fax: (415) 476-8173. E-mail: brian.black{at}ucsf.edu

{triangledown} Published ahead of print on 11 June 2007.

{dagger} Supplemental material for this article may be found at http://mcb.asm.org/.

Molecular and Cellular Biology, August 2007, p. 5910-5920, Vol. 27, No. 16
0270-7306/07/$08.00+0     doi:10.1128/MCB.01700-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

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