Fig. 7. Model for role of Dlx in positioning the neural plate border and patterning adjacent cell fates. (A) We postulate that a reciprocal (inhibitory) interaction between Dlx and neural plate factors refines an initial neural plate: non-neural ectoderm bias along the mediolateral axis. The initial bias is established earlier, possibly by BMP, Wnt and/or FGF signaling. This reciprocal interaction leads to a sharpening of the border between the neural plate and non-neural ectoderm and specifies the precise position along the mediolateral axis. (B-F) Schematics of ectoderm along the mediolateral axis illustrate the function of Dlx factors under normal and manipulated conditions. (B) Under normal conditions, Dlx activity is required in non-neural ectoderm (yellow) for short-range communication (arrows) that leads to induction of lateral primary neuron, neural crest and cranial placode precursors. (C) Local inhibition of Dlx activity within the region expressing injected EnR-Dlx3hd (red bars) causes the neural plate to expand. Border region cell lineages are induced laterally where the expanded neural plate contacts Dlx-positive non-neural ectoderm. (D) When Dlx3 activity is inhibited beyond the intrinsic limit of neural plate expansion, the neural plate expands maximally but is separated from Dlx-positive epidermis. Short-range communication is attenuated or not initiated, resulting in absence of neural crest, cranial placodes and lateral primary neurons. (E) Overexpression of Dlx activity (with VP16-Dlx3hd or full-length Dlx3) inhibits neural plate induction but cannot initiate epidermal differentiation (Fig. 2); thus, the neural plate narrows but short-range signaling and normal cell fate specification does not occur in the border region. (F) Cranial placodes can be shifted medially in cases where a small region of ectopic Dlx activity separates competent neural plate and non-neural ectoderm, suggesting that placode-inducing signals can traverse a short region of interposing tissue.

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