Fig. 11. A model for interactions between Fgf, Wnt and RA signaling in the neural ectoderm during gastrulation. (A) Sequence of posteriorization signals. Fgf and/or Wnt signals initiate the first step of posteriorization by suppressing expression of anterior genes, represented here by cyp26 and otx2. This process is not mediated by RA. In the posterior domain, where cyp26 expression is suppressed by Fgfs/Wnts, RA accumulates at least in part due to the activity of Raldh2, and activates posterior genes such as hoxb1b and meis3. (B) At the late blastula stage, Fgfs/Wnts are expressed in the mesoderm at the blastoderm margin. Fgf/Wnt signals from the margin block the expression of cyp26 in the adjacent ectoderm, which will give rise to the posterior neural plate. cyp26 is expressed in the anterior domain, at a distance from the source of the Fgf/Wnt signals; as a consequence, RA is degraded and the expression of posterior genes is prevented. After the beginning of gastrulation, convergence-extension movements lead to a widening of the cyp26-negative area, allowing RA to accumulate to a level where it can activate posterior genes such as hoxb1b. Subsequent cell movements expand the domain that will give rise to the posterior neural ectoderm.

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