Fig. 8.
Re-specification of the dorsal neural tube domain in the absence of Notch signaling. a–l In situ hybridization of transverse sections through the neural tube at the level of the forelimb in wildtype (WT) and Wnt1-Cre; Mib1fl/fl mouse embryos. Math1 expression at E10.5 (a, b) and E11.5 (c, d) showing loss of dI1 population in mutants; Ngn1 expression at E10.5 (e, f) and E11.5 (g, h) and Ngn2 expression at E10.5 (i, j) and E11.5 (k, l) showing dorsal-ward expansion of the dI2 population. m–x Immunostaining of transverse sections through the dorsal neural tube at the level of the forelimb in wildtype (WT) and Wnt1-Cre; Mib1fl/fl mouse embryos. Isl1 expression at E10.5 (m, n) and E11.5 (o, p) showing a dorsal-ward expansion of dI3 interneurons at E11.5 (arrows); AP2α expression at E10.5 (q, r) and E11.5 (s, t) showing a dorsal-ward expansion in mutants at both stages (positive staining within the neural tube lumen in T is due to erythrocyte autofluorescence); Tuj1 expression at E10.5 (u, v) and E11.5 (w, x) showing ectopic expression of the axonal marker Tuj1 in the dorsal neural tube of mutants. y, z Quantification of dI interneuron subtypes in the dorsal neural tube at E10.5 and E11.5. Isl1-positive dI3 interneuron numbers are unchanged in Wnt1-Cre; Mib1fl/fl embryos (y), whereas AP2α-positive dI2-5 interneuron numbers are increased in Wnt1-Cre; Mib1fl/fl embryos at both E10.5 and E11.5 (z). N = 3–4 embryos; ns, not significant; *p = 0.022; ***p = 0.0001. Bar = 50 μm