The Notch signaling pathway: Molecular basis of cell context dependency

Schwanbeck, Ralf; Martini, Simone; Bernoth, Kristina; Just, Ursula

doi:10.1016/j.ejcb.2010.10.004

Cited by 91 publications

(100 citation statements)

References 95 publications

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“…it is influenced by cross-talk with other signalling pathways and/or the cellular state (Hurlbut et al, 2007;Schwanbeck et al, 2011). In the present study, we observe actively dividing NICD-expressing stem/progenitor cells during embryonic stages and cell cyclearrested cells during late foetal myogenesis, although differentiation is blocked at both stages.…”

Section: Discussionmentioning

confidence: 59%

Cell-autonomous Notch activity maintains the temporal specification potential of skeletal muscle stem cells

et al. 2012

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SUMMARYDuring organogenesis, a continuum of founder stem cells produces temporally distinct progeny until development is complete. Similarly, in skeletal myogenesis, phenotypically and functionally distinct myoblasts and differentiated cells are generated during development. How this occurs in muscle and other tissues in vertebrates remains largely unclear. We showed previously that committed cells are required for maintaining muscle stem cells. Here we show that active Notch signalling specifies a subpopulation of myogenic cells with high Pax7 expression. By genetically modulating Notch activity, we demonstrate that activated Notch (NICD) blocks terminal differentiation in an Rbpj-dependent manner that is sufficient to sustain stem/progenitor cells throughout embryogenesis, despite the absence of committed progeny. Although arrested in lineage progression, NICDexpressing cells of embryonic origin progressively mature and adopt characteristics of foetal myogenic cells, including expression of the foetal myogenesis regulator Nfix. siRNA-mediated silencing of NICD promotes the temporally appropriate foetal myogenic fate in spite of expression of markers for multiple cell types. We uncover a differential effect of Notch, whereby high Notch activity is associated with stem/progenitor cell expansion in the mouse embryo, yet it promotes reversible cell cycle exit in the foetus and the appearance of an adult muscle stem cell state. We propose that active Notch signalling is sufficient to sustain an upstream population of muscle founder stem cells while suppressing differentiation. Significantly, Notch does not override other signals that promote temporal myogenic cell fates during ontology where spatiotemporal developmental cues produce distinct phenotypic classes of myoblasts.

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Section: Discussionmentioning

confidence: 59%

Cell-autonomous Notch activity maintains the temporal specification potential of skeletal muscle stem cells

et al. 2012

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“…Supporting this idea, we have recently shown the potential binding sites of RBP-J within the Sox9 promoter. 13,28 Sox9 was highly inducible by activated Notch1 during early EB differentiation, but not at late time points of differentiation (day 10; Figure 2b). Furthermore, to show the direct nature of Sox9 regulation by Notch1, we used luciferase reporter constructs that were transiently transfected into ES cells.…”

Section: Resultsmentioning

confidence: 99%

Notch1 signaling regulates chondrogenic lineage determination through Sox9 activation

et al. 2011

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“…1,2 The name "Notch" dates back as early as 1914, when a Drosophila female was described as having "notched" wings, which we now know results from a dominant haploinsufficiency of the gene. 3 One of the best-characterized examples of specific Notch function is lateral inhibition of neural/epidermal fate during Drosophila neurogenesis.…”

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confidence: 99%

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2012

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The Notch signaling pathway: Molecular basis of cell context dependency

Cited by 91 publications

References 95 publications

Cell-autonomous Notch activity maintains the temporal specification potential of skeletal muscle stem cells

Cell-autonomous Notch activity maintains the temporal specification potential of skeletal muscle stem cells

Notch1 signaling regulates chondrogenic lineage determination through Sox9 activation

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