Loss of Ptpn11 (Shp2) drives satellite cells into quiescence
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 combi...
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| Format: | Article |
| Language: | English |
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eLife Sciences Publications Ltd
2017-05-01
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| Series: | eLife |
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| Online Access: | https://elifesciences.org/articles/21552 |
| _version_ | 1811200859451686912 |
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| author | Joscha Griger Robin Schneider Ines Lahmann Verena Schöwel Charles Keller Simone Spuler Marc Nazare Carmen Birchmeier |
| author_facet | Joscha Griger Robin Schneider Ines Lahmann Verena Schöwel Charles Keller Simone Spuler Marc Nazare Carmen Birchmeier |
| author_sort | Joscha Griger |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-04-12T02:12:00Z |
| format | Article |
| id | doaj.art-15880a2efeb34a48b889ace679e7abcc |
| institution | Directory Open Access Journal |
| issn | 2050-084X |
| language | English |
| last_indexed | 2024-04-12T02:12:00Z |
| publishDate | 2017-05-01 |
| publisher | eLife Sciences Publications Ltd |
| record_format | Article |
| series | eLife |
| spelling | doaj.art-15880a2efeb34a48b889ace679e7abcc2022-12-22T03:52:22ZengeLife Sciences Publications LtdeLife2050-084X2017-05-01610.7554/eLife.21552Loss of Ptpn11 (Shp2) drives satellite cells into quiescenceJoscha Griger0https://orcid.org/0000-0001-8666-3371Robin Schneider1Ines Lahmann2Verena Schöwel3Charles Keller4Simone Spuler5https://orcid.org/0000-0002-0155-1117Marc Nazare6Carmen Birchmeier7https://orcid.org/0000-0002-2041-8872Developmental Biology/Signal Transduction Group, Max Delbrück Center for Molecular Medicine (MDC) in the Helmholtz Society, Berlin, GermanyDevelopmental Biology/Signal Transduction Group, Max Delbrück Center for Molecular Medicine (MDC) in the Helmholtz Society, Berlin, GermanyDevelopmental Biology/Signal Transduction Group, Max Delbrück Center for Molecular Medicine (MDC) in the Helmholtz Society, Berlin, GermanyMuscle Research Unit, Experimental and Clinical Research Center, Charité Medical Faculty and Max Delbrück Center for Molecular Medicine Berlin, Berlin, GermanyChildren's Cancer Therapy Development Institute, Beaverton, United StatesMuscle Research Unit, Experimental and Clinical Research Center, Charité Medical Faculty and Max Delbrück Center for Molecular Medicine Berlin, Berlin, GermanyMedicinal Chemistry, Leibniz Institute for Molecular Pharmacology, Berlin, GermanyDevelopmental Biology/Signal Transduction Group, Max Delbrück Center for Molecular Medicine (MDC) in the Helmholtz Society, Berlin, GermanyThe 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.https://elifesciences.org/articles/21552Shp2Ptpn11satellite cellsskeletal muscle repairskeletal muscle growthquiescence |
| spellingShingle | Joscha Griger Robin Schneider Ines Lahmann Verena Schöwel Charles Keller Simone Spuler Marc Nazare Carmen Birchmeier Loss of Ptpn11 (Shp2) drives satellite cells into quiescence eLife Shp2 Ptpn11 satellite cells skeletal muscle repair skeletal muscle growth quiescence |
| title | Loss of Ptpn11 (Shp2) drives satellite cells into quiescence |
| title_full | Loss of Ptpn11 (Shp2) drives satellite cells into quiescence |
| title_fullStr | Loss of Ptpn11 (Shp2) drives satellite cells into quiescence |
| title_full_unstemmed | Loss of Ptpn11 (Shp2) drives satellite cells into quiescence |
| title_short | Loss of Ptpn11 (Shp2) drives satellite cells into quiescence |
| title_sort | loss of ptpn11 shp2 drives satellite cells into quiescence |
| topic | Shp2 Ptpn11 satellite cells skeletal muscle repair skeletal muscle growth quiescence |
| url | https://elifesciences.org/articles/21552 |
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