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Coactosin-like protein 1 inhibits neuronal migration during mouse corticogenesis

机译:辅肌动蛋白样蛋白1抑制小鼠皮质发生过程中的神经元迁移。

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Coactosin-like protein 1 (Cotl1), a member of the actin-depolymerizing factor (ADF)/cofilin family, was first purified from a soluble fraction of Dictyostelium discoideum cells. Neuronal migration requires cytoskeletal remodeling and actin regulation. Although Cotl1 strongly binds to F-actin, the role of Cotl1 in neuronal migration remains undescribed. In this study, we revealed that Cotl1 overexpression impaired migrationof both early- and late-born neurons during mouse corticogenesis. Moreover, Cotl1 overexpression delayed, rather than blocked, neuronal migration in late-born neurons. Cotl1 expression disturbed the morphology of migrating neurons, lengthening the leading processes. This study is the first to investigate the function of Cotl1, and the results indicate that Cotl1 is involved in the regulation of neuronal migration and morphogenesis.
机译:肌动蛋白样蛋白1(Cotl1)是肌动蛋白解聚因子(ADF)/ cofilin家族的成员,首先从Disctyostelium discoideum细胞的可溶性级分中纯化出来。神经元迁移需要细胞骨架重塑和肌动蛋白调节。尽管Cotl1牢固地绑定到F-肌动蛋白,但Cotl1在神经元迁移中的作用仍未描述。在这项研究中,我们揭示了Cotl1的过表达会损害小鼠皮质发生过程中早期和晚期出生的神经元的迁移。此外,Cot1的过度表达延迟而不是阻止了晚期神经元的神经元迁移。 Cotl1表达扰乱了迁移神经元的形态,延长了主导进程。这项研究是第一个研究Cotl1的功能,结果表明Cotl1参与神经元迁移和形态发生的调节。

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