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Elife. 2017 May 2;6. pii: e21552. doi: 10.7554/eLife.21552.

Loss of Ptpn11 (Shp2) drives satellite cells into quiescence.

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Developmental Biology/Signal Transduction Group, Max Delbrück Center for Molecular Medicine (MDC) in the Helmholtz Society, Berlin, Germany.
Muscle Research Unit, Experimental and Clinical Research Center, Charité Medical Faculty and Max Delbrück Center for Molecular Medicine Berlin, Berlin, Germany.
Children's Cancer Therapy Development Institute, Beaverton, United States.
Medicinal Chemistry, Leibniz Institute for Molecular Pharmacology, Berlin, Germany.


The equilibrium between proliferation and quiescence of myogenic progenitor and stem cells is tightly regulated to ensure appropriate skeletal muscle growth and repair. The non-receptor tyrosine phosphatase Ptpn11 (Shp2) is an important transducer of growth factor and cytokine signals. Here we combined complex genetic analyses, biochemical studies and pharmacological interference to demonstrate a central role of Ptpn11 in postnatal myogenesis of mice. Loss of Ptpn11 drove muscle stem cells out of the proliferative and into a resting state during muscle growth. This Ptpn11 function was observed in postnatal but not fetal myogenic stem cells. Furthermore, muscle repair was severely perturbed when Ptpn11 was ablated in stem cells due to a deficit in stem cell proliferation and survival. Our data demonstrate a molecular difference in the control of cell cycle withdrawal in fetal and postnatal myogenic stem cells, and assign to Ptpn11 signaling a key function in satellite cell activity.


Ptpn11; Shp2; developmental biology; mouse; quiescence; satellite cells; skeletal muscle growth; skeletal muscle repair; stem cells

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