Reelin and cofilin cooperate during the migration of cortical neurons: a quantitative morphological analysis
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Reelin and cofilin cooperate during the migration of cortical neurons: a quantitative morphological analysis. / Chai, Xuejun; Zhao, Shanting; Fan, Li; Zhang, Wei; Lu, Xi; Shao, Hong; Wang, Shaobo; Song , Lingzhen ; Failla, Antonio Virgilio; Zobiak, Bernd; Mannherz, Hans G; Frotscher, Michael.
in: DEVELOPMENT, Jahrgang 143, Nr. 6, 15.03.2016, S. 1029-40.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Reelin and cofilin cooperate during the migration of cortical neurons: a quantitative morphological analysis
AU - Chai, Xuejun
AU - Zhao, Shanting
AU - Fan, Li
AU - Zhang, Wei
AU - Lu, Xi
AU - Shao, Hong
AU - Wang, Shaobo
AU - Song , Lingzhen
AU - Failla, Antonio Virgilio
AU - Zobiak, Bernd
AU - Mannherz, Hans G
AU - Frotscher, Michael
N1 - © 2016. Published by The Company of Biologists Ltd.
PY - 2016/3/15
Y1 - 2016/3/15
N2 - In reeler mutant mice, which are deficient in reelin (Reln), the lamination of the cerebral cortex is disrupted. Reelin signaling induces phosphorylation of LIM kinase 1, which phosphorylates the actin-depolymerizing protein cofilin in migrating neurons. Conditional cofilin mutants show neuronal migration defects. Thus, both reelin and cofilin are indispensable during cortical development. To analyze the effects of cofilin phosphorylation on neuronal migration we used in utero electroporation to transfect E14.5 wild-type cortical neurons with pCAG-EGFP plasmids encoding either a nonphosphorylatable form of cofilin 1 (cofilin(S3A)), a pseudophosphorylated form (cofilin(S3E)) or wild-type cofilin 1 (cofilin(WT)). Wild-type controls and reeler neurons were transfected with pCAG-EGFP. Real-time microscopy and histological analyses revealed that overexpression of cofilin(WT) and both phosphomutants induced migration defects and morphological abnormalities of cortical neurons. Of note, reeler neurons and cofilin(S3A)- and cofilin(S3E)-transfected neurons showed aberrant backward migration towards the ventricular zone. Overexpression of cofilin(S3E), the pseudophosphorylated form, partially rescued the migration defect of reeler neurons, as did overexpression of Limk1. Collectively, the results indicate that reelin and cofilin cooperate in controlling cytoskeletal dynamics during neuronal migration.
AB - In reeler mutant mice, which are deficient in reelin (Reln), the lamination of the cerebral cortex is disrupted. Reelin signaling induces phosphorylation of LIM kinase 1, which phosphorylates the actin-depolymerizing protein cofilin in migrating neurons. Conditional cofilin mutants show neuronal migration defects. Thus, both reelin and cofilin are indispensable during cortical development. To analyze the effects of cofilin phosphorylation on neuronal migration we used in utero electroporation to transfect E14.5 wild-type cortical neurons with pCAG-EGFP plasmids encoding either a nonphosphorylatable form of cofilin 1 (cofilin(S3A)), a pseudophosphorylated form (cofilin(S3E)) or wild-type cofilin 1 (cofilin(WT)). Wild-type controls and reeler neurons were transfected with pCAG-EGFP. Real-time microscopy and histological analyses revealed that overexpression of cofilin(WT) and both phosphomutants induced migration defects and morphological abnormalities of cortical neurons. Of note, reeler neurons and cofilin(S3A)- and cofilin(S3E)-transfected neurons showed aberrant backward migration towards the ventricular zone. Overexpression of cofilin(S3E), the pseudophosphorylated form, partially rescued the migration defect of reeler neurons, as did overexpression of Limk1. Collectively, the results indicate that reelin and cofilin cooperate in controlling cytoskeletal dynamics during neuronal migration.
KW - Animals
KW - Cell Adhesion Molecules, Neuronal
KW - Cell Count
KW - Cell Movement
KW - Cell Shape
KW - Cerebral Cortex
KW - Cofilin 1
KW - Electroporation
KW - Embryo, Mammalian
KW - Extracellular Matrix Proteins
KW - Female
KW - Mice, Inbred C57BL
KW - Nerve Tissue Proteins
KW - Neurons
KW - Serine Endopeptidases
KW - Transfection
KW - Journal Article
KW - Research Support, Non-U.S. Gov't
U2 - 10.1242/dev.134163
DO - 10.1242/dev.134163
M3 - SCORING: Journal article
C2 - 26893343
VL - 143
SP - 1029
EP - 1040
JO - DEVELOPMENT
JF - DEVELOPMENT
SN - 0950-1991
IS - 6
ER -