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Mouse Fyn induces pseudopodium formation in Chinese hamster ovary cells
Lei An,Shengnan Liu,Wei Zhang,Yamei Zhang,Yingxue Huang,Xinde Hu,Shu-lin Chen,Shanting Zhao 대한수의학회 2014 JOURNAL OF VETERINARY SCIENCE Vol.15 No.1
Molecular mechanisms underlying the effects of Fyn on cellmorphology, pseudopodium movement, and cell migrationwere investigated. The Fyn gene was subcloned into pEGFP-N1to produce pEGFP-N1-Fyn. Chinese hamster ovary (CHO)cells were transfected with pEGFP-N1-Fyn. The expression ofFyn mRNA and proteins was monitored by reversetranscription-PCR and Western blotting. Additionally,transfected cells were stained with 4´,6-diamidino-2-phenylindole and a series of time-lapse images was taken. Sequences of the recombinant plasmids pMD18-T-Fyn andpEGFP-N1-Fyn were confirmed by sequence identificationusing National Center for Biotechnology Information in USA,and Fyn expression was detected by RT-PCR and Westernblotting. The morphology of CHO cells transfected with therecombinant vector was significantly altered. Fyn expressioninduced filopodia and lamellipodia formation. Based on theseresults, we concluded that overexpression of mouse Fyn inducesthe formation of filopodia and lamellipodia in CHO cells, andpromotes cell movement.
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 대한수의학회 2018 Journal of Veterinary Science Vol.19 No.1
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.