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Coactosin-like protein-1 inhibits the 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, Shanxi, China
Correspondence to: 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: April 6, 2017.
Abstract
Coactosin-like protein-1 (Cotl1), a member of the actin-depolymerizing factor (ADF)/cofilin family, was first purified from the 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 unknown. Here, we revealed that Cotl1 overexpression impaired the migration of 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, thus lengthening the leading processes. This study is the first to investigate the function of Cotl1 in vivo. Results indicated that Cotl1 is involved in the regulation of neuronal migration and morphogenesis.
Keywords: Cotl1; actin; in utero electroporation; neuronal migration


© 2017 The Korean Society of Veterinary Science.