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Loss of Ptpn11 (Shp2) drives satellite cells into quiescence

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Item Type:Article
Title:Loss of Ptpn11 (Shp2) drives satellite cells into quiescence
Creators Name:Griger, J. and Schneider, R. and Lahmann, I. and Schöwel, V. and Keller, C. and Spuler, S. and Nazare, M. and Birchmeier, C.
Abstract:The equilibrium between proliferation and quiescence of myogenic progenitor and stem cells is tightly regulated to ensure appropriate 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.
Keywords:Cytokines, Intercellular Signaling Peptides and Proteins, Protein Tyrosine Phosphatase, Non-Receptor Type 11, Satellite Cells, Skeletal Muscle, Signal Transduction, Animals, Mice, Inbred C57BL
Publisher:eLife Sciences Publications
Page Range:e21552
Date:2 May 2017
Official Publication:https://doi.org/10.7554/eLife.21552
PubMed:View item in PubMed

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