Genome wide expression analysis of FACS-isolated Shp2 mutant neonatal myogenic progenitor cells

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 Shp2 (Ptpn11) is an important transducer of growth factor and cytokine signaling. Here we combined complex genetic analyses, biochemical studies and pharmacological interference to demonstrate a central role of Shp2 in postnatal myogenesis of mice. Loss of Shp2 drove muscle stem cells into quiescence during postnatal muscle growth and repair and thus interfered with myogenesis in a drastic manner. This Shp2 function was observed in postnatal but not fetal myogenic stem cells. Thus, we provide evidence for an unexpected molecular difference in the control of proliferation and cell cycle withdrawal in fetal and postnatal myogenic stem cells. Total RNA was obtained from VCAM1+CD31-CD45-Sca1- cells isolated from newborn control and coShp2 mice (P0) by FACS