Fig. 9.

Role/s of Notch signaling in RP/interneuron development. a–c Gain of Notch activity in quail embryos. In controls (a), the RP (red) is flanked by adjacent dorsal interneurons (dI1, yellow). b Missexpression of active Notch (green) in RP prevents expression of RP-specific traits in a cell-autonomous manner while upregulating BarHL1, a marker of dI1 interneurons. c Missexpression of active Notch ventral to the RP suppresses dI1 interneuron fate while upregulating RP markers in adjacent cells. d, e Wild type (WT) mouse embryo showing the RP flanked bilaterally by dI1 and dI2 interneurons (d). Loss of Notch function in Wnt1-Cre; Mib1 mutants prevents the development of RP and of dI1 interneurons, with a corresponding dorsal expansion of the dI2 interneuron population (E, orange). f At the trunk level of the axis, a sharp boundary between non-RP (blue) and RP (red) is demarcated by the dorsal extent of Notch activity (arrowhead). Notch signaling from this domain acts either directly or indirectly to induce RP formation (arrow 1 in left side of the image) and the RP in turn induces dorsal interneurons (arrow 2, IN). Alternatively, this boundary acts bidirectionally to induce both RP and INs (dotted arrows, right side). See text for detailed discussion