Li Guohong, Yin Yupeng, Chen Jiong, Fan Yanle, Ma Juhong, Huang Yingxue, Chen Chen, Dai Pengxiu, Chen Shulin, Zhao Shanting
College of Veterinary Medicine, Northwest A&F University, Yangling 712100, China.
J Vet Sci. 2018 Jan 31;19(1):21-26. doi: 10.4142/jvs.2018.19.1.21.
Coactosin-like protein 1 (Cotl1), a member of the actin-depolymerizing factor (ADF)/cofilin family, was first purified from a soluble fraction of 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.
类肌动蛋白解聚因子蛋白1（Cotl1）是肌动蛋白解聚因子（ADF）/丝切蛋白家族的成员之一，最初是从细胞的可溶性组分中纯化得到的。神经元迁移需要细胞骨架重塑和肌动蛋白调节。尽管Cotl1与F-肌动蛋白紧密结合，但其在神经元迁移中的作用仍未得到描述。在本研究中，我们发现Cotl1过表达会损害小鼠皮质发生过程中早出生和晚出生神经元的迁移。此外，Cotl1过表达会延迟而非阻断晚出生神经元的迁移。Cotl1表达扰乱了迁移神经元的形态，延长了前端突起。本研究首次探究了Cotl1的功能，结果表明Cotl1参与了神经元迁移和形态发生的调节。
