Mena is required for neurulation and commissure formation
Mena is required for neurulation and commissure formation
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DOI：
10.1016/s0896-6273(00)81092-2
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发表时间：
1999-02-01
期刊：
影响因子：
16.2
通讯作者：
Gertler, FB
中科院分区：
文献类型：
--
作者：
Lanier, LM;Gates, MA;Gertler, FB
哺乳动物启用 (Mena) 是蛋白质家族的成员，该蛋白质家族被认为将信号转导途径与肌动蛋白细胞骨架的局部重塑联系起来。 Mena 直接与 Profilin 结合，Profilin 是一种调节肌动蛋白聚合的肌动蛋白结合蛋白。在初级神经元中，Mena 集中在生长锥丝状伪足的尖端。 Mena 缺陷小鼠可以存活；然而，在早期新生儿中，从半球间皮质-皮质神经元投射的轴突走错了路线，而在成人中胼胝体交叉失败以及海马连合和脑桥小脑通路的缺陷也很明显。 Profilin I 缺失杂合的 Mena 缺陷小鼠会在子宫内死亡，并表现出神经发育缺陷，这表明 Mena 在肌动蛋白细胞骨架调节中发挥着重要的功能作用。
Mammalian enabled (Mena) is a member of a protein family thought to link signal transduction pathways to localized remodeling of the actin cytoskeleton. Mena binds directly to Profilin, an actin-binding protein that modulates actin polymerization. In primary neurons, Mena is concentrated at the tips of growth cone filopodia. Mena-deficient mice are viable; however, axons projecting from interhemispheric cortico-cortical neurons are misrouted in early neonates, and failed decussation of the corpus callosum as well as defects in the hippocampal commissure and the pontocerebellar pathway are evident in the adult. Mena-deficient mice that are heterozygous for a Profilin I deletion die in utero and display defects in neurulation, demonstrating an important functional role for Mena in regulation of the actin cytoskeleton.