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Published online June 4, 2007
doi:10.1083/jcb.200608122
The Journal of Cell Biology, Vol. 177, No. 5, 769-779
The Rockefeller University Press, 0021-9525 $30.00
© 2007 Olguin et al.
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Article

Reciprocal inhibition between Pax7 and muscle regulatory factors modulates myogenic cell fate determination



Hugo C. Olguin1, Zhihong Yang2, Stephen J. Tapscott2, and Bradley B. Olwin1

1 Department of Molecular, Cellular and Developmental Biology, University of Colorado, Boulder, CO 80309
2 Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, WA 98109

Correspondence to Bradley B. Olwin: Bradley.Olwin{at}colorado.edu

Postnatal growth and regeneration of skeletal muscle requires a population of resident myogenic precursors named satellite cells. The transcription factor Pax7 is critical for satellite cell biogenesis and survival and has been also implicated in satellite cell self-renewal; however, the underlying molecular mechanisms remain unclear. Previously, we showed that Pax7 overexpression in adult primary myoblasts down-regulates MyoD and prevents myogenin induction, inhibiting myogenesis. We show that Pax7 prevents muscle differentiation independently of its transcriptional activity, affecting MyoD function. Conversely, myogenin directly affects Pax7 expression and may be critical for Pax7 down-regulation in differentiating cells. Our results provide evidence for a cross-inhibitory interaction between Pax7 and members of the muscle regulatory factor family. This could represent an additional mechanism for the control of satellite cell fate decisions resulting in proliferation, differentiation, and self-renewal, necessary for skeletal muscle maintenance and repair.

Abbreviations used in this paper: EMSA, electrophoretic mobility shift assay; MRF, muscle regulatory factor; MyHC, myosin heavy chain.


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