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Published 11 April 2005. doi:10.1083/jcb.200408066
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 169, Number 1, 105-116
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Article

 The p38{alpha}/ß MAPK functions as a molecular switch to activate the quiescent satellite cell

Nathan C. Jones1, Kristina J. Tyner3, Lisa Nibarger3, Heather M. Stanley3, Dawn D.W. Cornelison3, Yuri V. Fedorov2, and Bradley B. Olwin3

1 Bayer Corporation, Research Triangle Park, NC 27709
2 Dharmacon Research, Lafayette, CO 80026
3 Department of Molecular, Cellular, and Developmental Biology, University of Colorado at Boulder, Boulder, CO 80309

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

Somatic stem cells cycle slowly or remain quiescent until required for tissue repair and maintenance. Upon muscle injury, stem cells that lie between the muscle fiber and basal lamina (satellite cells) are activated, proliferate, and eventually differentiate to repair the damaged muscle. Satellite cells in healthy muscle are quiescent, do not express MyoD family transcription factors or cell cycle regulatory genes and are insulated from the surrounding environment. Here, we report that the p38{alpha}/ß family of mitogen-activated protein kinases (MAPKs) reversibly regulates the quiescent state of the skeletal muscle satellite cell. Inhibition of p38{alpha}/ß MAPKs (a) promotes exit from the cell cycle, (b) prevents differentiation, and (c) insulates the cell from most external stimuli allowing the satellite cell to maintain a quiescent state. Activation of satellite cells and p38{alpha}/ß MAPKs occurs concomitantly, providing further support that these MAPKs function as a molecular switch for satellite cell activation.

N.C. Jones and K.J. Tyner contributed equally to this work.

Abbreviation used in this paper: ERK, extracellular signal-regulated kinase.


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