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¹ Institute of Cell Biology, Department of Biology, Swiss Federal Institute of Technology, ETH-Hönggerberg, CH-8093 Zurich, Switzerland
² Department of Genetics, University of Pennsylvania School of Medicine, Philadelphia, PA 19104
³ Research Laboratory for Calcium Metabolism, University Hospital Balgrist, University of Zurich, CH-8008 Zurich, Switzerland

Correspondence to Lukas Sommer: sommer{at}cell.biol.ethz.ch

Canonical Wnt signaling instructively promotes sensory neurogenesis in early neural crest stem cells (eNCSCs) (Lee, H.Y., M. Kléber, L. Hari, V. Brault, U. Suter, M.M. Taketo, R. Kemler, and L. Sommer. 2004. Science. 303:1020–1023). However, during normal development Wnt signaling induces a sensory fate only in a subpopulation of eNCSCs while other cells maintain their stem cell features, despite the presence of Wnt activity. Hence, factors counteracting Wnt signaling must exist. Here, we show that bone morphogenic protein (BMP) signaling antagonizes the sensory fate-inducing activity of Wnt/ß-catenin. Intriguingly, Wnt and BMP act synergistically to suppress differentiation and to maintain NCSC marker expression and multipotency. Similar to NCSCs in vivo, NCSCs maintained in culture alter their responsiveness to instructive growth factors with time. Thus, stem cell development is regulated by combinatorial growth factor activities that interact with changing cell-intrinsic cues.

Abbreviations used in this paper: BMP, bone morphogenic protein; DRG, dorsal root ganglia; eNCSC, early neural crest stem cell; GFAP, glial fibrillary acidic protein; NCSC, neural crest stem cell; NF, neurofilament; NRG, neuregulin; PNS, peripheral nervous system; SMA, smooth muscle actin.

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