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XB-IMG-84075

Xenbase Image ID: 84075

Fig. 9. Models for generic placode induction. (A) Four models have been proposed to explain the positioning of the neural crest, panplacodal primordium, and epidermis around the anterior neural plate. All models share the assumption that in a first step neural induction occurs by a signal (turquoise arrows) from the axial mesoderm (dark gray circle). The Delay model suggests that the slowly spreading neural inducer then reaches more lateral ectoderm after a time delay, during which ectodermal competence has changed in an autonomous fashion (more yellowish color). The Gradient model assumes that neural induction establishes a gradient of a morphogen (e.g., BMP; orange) followed by the specification of different ectodermal fates at different threshold concentrations. The Neural plate border state model proposes that a special neural plate border region (pink) is induced first followed by the induction of neural crest and panplacodal primordium by additional signals from adjacent ectoderm and mesoderm (blue and red arrows). Different versions of this model suggest (from left to right) that the neural plate border is established (1) by a morphogen gradient (orange), (2) by epidermal–neural interactions (pink arrows), or (3) by initial induction of a border state throughout the dorsal ectoderm followed by induction of a proper neural plate in the center (green arrows). The Binary competence model suggests that neural induction establishes a dorsal ectodermal competence region (possibly at a particular threshold of a BMP gradient), which maintains competence (light green) to form neural plate and neural crest and has a neural default fate, while ventral ectoderm cell-autonomously loses neural/neural crest competence but retains competence (light yellow) to adopt epidermal or placodal fates and has an epidermal default fate. Subsequently, additional signals from adjacent ectoderm and mesoderm induce neural crest and panplacodal primordium (blue and red arrows). (B) Summary of tissues and signals involved in induction of neural crest (left side; blue arrows and bars) and panplacodal primordium (right side, red arrows and bars) from the perspective of the Binary competence model. In addition to the cranial neural plate, its continuation into upper trunk levels is depicted. Whereas signals from prospective epidermis, neural plate border region, and paraxial mesoderm including Wnts, FGFs, and BMPs induce neural crest at the border of the neural/neural crest competence region, FGFs together with BMP and Wnt antagonists from the anterior neural plate and the cranial dorsolateral endomesoderm induce the panplacodal primordium at the border of the epidermal/placodal competence region. Because neural crest is specified earlier than the panplacodal primordium, it may escape the action of BMP and Wnt antagonists from the neural plate. Note that in this model differential ectodermal competence of the dorsal and ventral ectodermal territories defines the ventral limit of neural crest induction and the dorsal limit of generic placode induction. The ventral and posterior limits of generic placode induction are probably imposed by the extent of the signaling center producing BMP and Wnt antagonists in the cranial dorsolateral endomesoderm, which protects the overlying ectoderm from BMP and Wnt signals only in the dorsolateral head region. In contrast, the dorsal limits of neural crest induction may be set by thresholds of availability of the signals (Wnts, BMP, FGF) required for neural crest induction, while the anterior limits of crest induction are probably imposed by an unknown repressing signal that is rostrally confined.

Image published in: Schlosser G (2006)

Copyright © 2006. Image reproduced on Xenbase with permission of the Publisher, Elsevier B. V.

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