Vertebrate limbs originate from the lateral plate mesoderm (LPM) and the overlying ectoderm. While normal limb formation in defined regions has been well studied, the question of whether other positions retain limb-forming potential has not been fully investigated in mice. By ectopically activating β-catenin in the ectoderm with Msx2-cre, we observed that local tissue outgrowths were induced, which either progressed into limb-like structure within the inter-limb flank or formed extra tissues in other parts of the mouse embryo. In the presumptive abdominal region of severely affected embryos, ectopic limb formation was coupled with impaired abdominal ventral body wall (AVBW) closure, which indicates the existence of a potential counterbalance of limb formation and AVBW closure. At the molecular level, constitutive β-catenin activation was sufficient to trigger, but insufficient to maintain the ectopic expression of a putative limb-inducing factor, Fgf8, in the ectoderm. These findings provide new insight into the mechanism of limb formation and AVBW closure, and the crosstalk between the Wnt/β-catenin pathway and Fgf signal.

中文翻译：

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外胚层 β-连环蛋白的组成性激活诱导小鼠胚胎不同位置的异位生长，并影响腹部腹侧体壁闭合。

脊椎动物的四肢起源于侧板中胚层 (LPM) 和上覆的外胚层。虽然已对特定区域的正常肢体形成进行了充分研究，但尚未在小鼠中充分研究其他位置是否保留肢体形成潜力的问题。通过用 Msx2-cre 异位激活外胚层中的 β-连环蛋白，我们观察到局部组织生长被诱导，其要么在四肢间侧发展成肢状结构，要么在小鼠胚胎的其他部分形成额外的组织。在受严重影响的胚胎的推定腹部区域，异位肢体形成与腹部腹侧体壁 (AVBW) 闭合受损相结合，这表明存在肢体形成和 AVBW 闭合的潜在平衡。在分子水平上，组成型 β-连环蛋白激活足以触发，但不足以维持外胚层中假定的肢体诱导因子 Fgf8 的异位表达。这些发现为肢体形成和 AVBW 闭合的机制以及 Wnt/β-catenin 通路与 Fgf 信号之间的串扰提供了新的见解。