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. 2013 Apr 16;288(23):16655–16670. doi: 10.1074/jbc.M113.451070

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© 2013 by The American Society for Biochemistry and Molecular Biology, Inc.

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FIGURE 8. — Cubn promotes Fgf signaling in the chick CNCC and CE together with FgfR3. A–A″, overexpression of Noggin in the CNCC of dsCubn-treated embryos restores head morphology. B–C‴, representative gross (B–B‴) and brain (C–C‴) morphology of E5 embryos electroporated in the CNCC and CE with dsControl (B and C), dsFgfR3 (B′ and C′), dsFgfR1 (B″ and C″), and dsFgR2 (B‴ and C‴). Cephalic hypoplasia is observed exclusively in dsFgfR3-treated embryos (arrowhead points to the telencephalon). D–D″, extremely severe head hypoplasia in double dsCubn-dsFgfR3 electroporated embryos at E2 (D″) compared with dsCubn-treated embryos of the same stage (D′). E, proposed Cubn-Fgf8 interaction in the CNCC and CE. Cubn expressed at the plasma membrane binds extracellular Fgf8, favors its endocytosis (assisted by Lrp2 and/or a yet unknown partner), and increases its availability for FgfRs within the cell. Cubn-dependent FgfR activation together with Bmp antagonism, here via Noggin, is necessary to counter Bmp activity and promote CNCC and CE survival. Scale bars, A–C‴, 900 μm; D–D″, 100 μm.