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Published 7 November 2005. doi:10.1083/jcb.200502101
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 171, Number 3, 471-482
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Article

 MyoD induces myogenic differentiation through cooperation of its NH2- and COOH-terminal regions

Jeff Ishibashi1,2, Robert L. Perry3, Atsushi Asakura2, and Michael A. Rudnicki1,2,3

1 Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, Ontario K1N 6N5, Canada
2 Molecular Medicine Program, Ottawa Health Research Institute, Ottawa, Ontario K1H 8L6, Canada
3 Faculty of Health Sciences, McMaster University, Hamilton, Ontario L8N 3Z5, Canada

Correspondence to Michael A. Rudnicki: mrudnicki{at}ohri.ca

MyoD and Myf5 are basic helix-loop-helix transcription factors that play key but redundant roles in specifying myogenic progenitors during embryogenesis. However, there are functional differences between the two transcription factors that impact myoblast proliferation and differentiation. Target gene activation could be one such difference. We have used microarray and polymerase chain reaction approaches to measure the induction of muscle gene expression by MyoD and Myf5 in an in vitro model. In proliferating cells, MyoD and Myf5 function very similarly to activate the expression of likely growth phase target genes such as L-myc, m-cadherin, Mcpt8, Runx1, Spp1, Six1, IGFBP5, and Chrnß1. MyoD, however, is strikingly more effective than Myf5 at inducing differentiation-phase target genes. This distinction between MyoD and Myf5 results from a novel and unanticipated cooperation between the MyoD NH2- and COOH-terminal regions. Together, these results support the notion that Myf5 functions toward myoblast proliferation, whereas MyoD prepares myoblasts for efficient differentiation.

Abbreviations used in this paper: bHLH, basic helix-loop-helix; dblKO, double knockout; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; MRF, myogenic regulatory factor.


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