Abstract
Summary Despite recent explorations of tissue-level epithelial morphogenesis, how the embryonic brain wall, an epithelial derivative unique in its extensive cellular stratification coupled with epithelial-cell heightening to ∼0.5 mm, achieves thickening is unknown. Furthermore, the role of the inner curvature of the wall in this process remains unclear. Thus, whether the apically concave dorsal cerebral (pallial) wall thickens inward, not only outward as previously thought, was examined in culture and in vivo . The pallial wall in the midembryonic period, but not the earlier pallial wall, thickened inward at a pace equivalent to that of neuronal accumulation, which was found via stress-release tests to proceed in a compressive manner. The inhibition of actomyosin-mediated contraction of the inner/apical surface prevented the pallium from thickening, while inducing apical-surface buckling, suggesting the necessity of this inward thickening to actively avoid overcrowding. In contrast, inward bulging of the apically convex ganglionic eminence occurs more passively via pushing of the low-actomyosin apical surface by the constituent cells.
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Summary
Despite recent explorations of tissue-level epithelial morphogenesis, how the embryonic brain wall, an epithelial derivative unique in its extensive cellular stratification coupled with epithelial-cell heightening to ∼0.5 mm, achieves thickening is unknown. Furthermore, the role of the inner curvature of the wall in this process remains unclear. Thus, whether the apically concave dorsal cerebral (pallial) wall thickens inward, not only outward as previously thought, was examined in culture and in vivo. The pallial wall in the midembryonic period, but not the earlier pallial wall, thickened inward at a pace equivalent to that of neuronal accumulation, which was found via stress-release tests to proceed in a compressive manner. The inhibition of actomyosin-mediated contraction of the inner/apical surface prevented the pallium from thickening, while inducing apical-surface buckling, suggesting the necessity of this inward thickening to actively avoid overcrowding. In contrast, inward bulging of the apically convex ganglionic eminence occurs more passively via pushing of the low-actomyosin apical surface by the constituent cells.
Competing Interest Statement
The authors have declared no competing interest.
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