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J Vet Sci 2018; 19(1): 21-26  https://doi.org/10.4142/jvs.2018.19.1.21
Coactosin-like protein 1 inhibits neuronal migration during mouse corticogenesis
Guohong Li, Yupeng Yin, Jiong Chen, Yanle Fan, Juhong Ma, Yingxue Huang, Chen Chen, Pengxiu Dai, Shulin Chen*, Shanting Zhao*
College of Veterinary Medicine, Northwest A&F University, Yangling 712100, China
Correspondence to: Shulin Chen, Shanting Zhao
Tel/Fax: +86-29-87091117; E-mails: shantingzhao@hotmail.com (S Zhao), csl_1359@126.com (S Chen)
The first two authors contributed equally to this work.
Received: October 4, 2016; Revised: December 19, 2016; Accepted: February 7, 2017; Published online: January 31, 2018.
Abstract
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.
Keywords: Cotl1 protein, actins, in utero electroporation, neuronal migration


© 2018 The Korean Society of Veterinary Science.

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