4.3 Article

Coactosin-like protein 1 inhibits neuronal migration during mouse corticogenesis

Journal

JOURNAL OF VETERINARY SCIENCE
Volume 19, Issue 1, Pages 21-26

Publisher

KOREAN SOC VETERINARY SCIENCE
DOI: 10.4142/jvs.2018.19.1.21

Keywords

Cotl1 protein; actins; in utero electroporation; neuronal migration

Funding

  1. National Natural Science Foundation of China [31301970]
  2. Postdoctoral Science Foundation of China [2015M570858]
  3. Fundamental Research Funds for the Central Universities [2452015039]
  4. Natural Science Foundation of Shaanxi [2016JM3033]
  5. Resource-based Industry Key Technology Project of Shaanxi Province [2016KTCL02-19]

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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 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, 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.

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