Role for Reelin-induced cofilin phosphorylation in the assembly of sympathetic preganglionic neurons in the murine intermediolateral column.

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Role for Reelin-induced cofilin phosphorylation in the assembly of sympathetic preganglionic neurons in the murine intermediolateral column. / Krüger, Marie T; Zhao, Shanting; Chai, Xuejun; Brunne, Bianka; Bouché, Elisabeth; Bock, Hans H; Frotscher, Michael.

In: EUR J NEUROSCI, Vol. 32, No. 10, 10, 2010, p. 1611-1617.

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@article{b557eba678034a039a8135dd95cff245,
title = "Role for Reelin-induced cofilin phosphorylation in the assembly of sympathetic preganglionic neurons in the murine intermediolateral column.",
abstract = "Sympathetic preganglionic neurons (SPNs) are located in the intermediolateral column (IMLC) of the spinal cord. This specific localization results from primary and secondary migratory processes during spinal cord development. Thus, following neurogenesis in the neuroepithelium, SPNs migrate first in a ventrolateral direction and then, in a secondary step, dorsolaterally to reach the IMLC. These migratory processes are controlled, at least in part, by the glycoprotein Reelin, which is known to be important for the development of laminated brain structures. In reeler mutants deficient in Reelin, SPNs initially migrate ventrolaterally as normal. However, most of them then migrate medially to become eventually located near the central canal. Here, we provide evidence that in wild-type animals this aberrant medial migration towards the central canal is prevented by Reelin-induced cytoskeletal stabilization, brought about by phosphorylation of cofilin. Cofilin plays an important role in actin depolymerization, a process required for the changes in cell shape during migration. Phosphorylation of cofilin renders it unable to depolymerize F-actin, thereby stabilizing the cytoskeleton. Using immunostaining for phosphorylated cofilin (p-cofilin), we demonstrate that SPNs in wild-type animals, but not in reeler mutants and other mutants of the Reelin signalling cascade, are immunoreactive for p-cofilin. These findings suggest that Reelin near the central canal induces cofilin phosphorylation in SPNs, thereby preventing them from aberrant migration towards the central canal. The results extend our previous studies on cortical neurons in which Reelin in the marginal zone was found to stabilize the leading processes of migrating neurons and terminate the migration process.",
keywords = "Animals, Mice, Mice, Knockout, Staining and Labeling methods, histology, Phosphorylation, Neurons cytology, Mice, Neurologic Mutants, Receptors, LDL genetics, Cell Adhesion Molecules, Neuronal genetics, Extracellular Matrix Proteins genetics, Nerve Tissue Proteins genetics, Serine Endopeptidases genetics, Actin Depolymerizing Factors genetics, Autonomic Fibers, Preganglionic metabolism, Ganglia, Sympathetic cytology, Spinal Cord anatomy, Animals, Mice, Mice, Knockout, Staining and Labeling methods, histology, Phosphorylation, Neurons cytology, Mice, Neurologic Mutants, Receptors, LDL genetics, Cell Adhesion Molecules, Neuronal genetics, Extracellular Matrix Proteins genetics, Nerve Tissue Proteins genetics, Serine Endopeptidases genetics, Actin Depolymerizing Factors genetics, Autonomic Fibers, Preganglionic metabolism, Ganglia, Sympathetic cytology, Spinal Cord anatomy",
author = "Kr{\"u}ger, {Marie T} and Shanting Zhao and Xuejun Chai and Bianka Brunne and Elisabeth Bouch{\'e} and Bock, {Hans H} and Michael Frotscher",
year = "2010",
language = "Deutsch",
volume = "32",
pages = "1611--1617",
journal = "EUR J NEUROSCI",
issn = "0953-816X",
publisher = "Wiley-Blackwell",
number = "10",

}

RIS

TY - JOUR

T1 - Role for Reelin-induced cofilin phosphorylation in the assembly of sympathetic preganglionic neurons in the murine intermediolateral column.

AU - Krüger, Marie T

AU - Zhao, Shanting

AU - Chai, Xuejun

AU - Brunne, Bianka

AU - Bouché, Elisabeth

AU - Bock, Hans H

AU - Frotscher, Michael

PY - 2010

Y1 - 2010

N2 - Sympathetic preganglionic neurons (SPNs) are located in the intermediolateral column (IMLC) of the spinal cord. This specific localization results from primary and secondary migratory processes during spinal cord development. Thus, following neurogenesis in the neuroepithelium, SPNs migrate first in a ventrolateral direction and then, in a secondary step, dorsolaterally to reach the IMLC. These migratory processes are controlled, at least in part, by the glycoprotein Reelin, which is known to be important for the development of laminated brain structures. In reeler mutants deficient in Reelin, SPNs initially migrate ventrolaterally as normal. However, most of them then migrate medially to become eventually located near the central canal. Here, we provide evidence that in wild-type animals this aberrant medial migration towards the central canal is prevented by Reelin-induced cytoskeletal stabilization, brought about by phosphorylation of cofilin. Cofilin plays an important role in actin depolymerization, a process required for the changes in cell shape during migration. Phosphorylation of cofilin renders it unable to depolymerize F-actin, thereby stabilizing the cytoskeleton. Using immunostaining for phosphorylated cofilin (p-cofilin), we demonstrate that SPNs in wild-type animals, but not in reeler mutants and other mutants of the Reelin signalling cascade, are immunoreactive for p-cofilin. These findings suggest that Reelin near the central canal induces cofilin phosphorylation in SPNs, thereby preventing them from aberrant migration towards the central canal. The results extend our previous studies on cortical neurons in which Reelin in the marginal zone was found to stabilize the leading processes of migrating neurons and terminate the migration process.

AB - Sympathetic preganglionic neurons (SPNs) are located in the intermediolateral column (IMLC) of the spinal cord. This specific localization results from primary and secondary migratory processes during spinal cord development. Thus, following neurogenesis in the neuroepithelium, SPNs migrate first in a ventrolateral direction and then, in a secondary step, dorsolaterally to reach the IMLC. These migratory processes are controlled, at least in part, by the glycoprotein Reelin, which is known to be important for the development of laminated brain structures. In reeler mutants deficient in Reelin, SPNs initially migrate ventrolaterally as normal. However, most of them then migrate medially to become eventually located near the central canal. Here, we provide evidence that in wild-type animals this aberrant medial migration towards the central canal is prevented by Reelin-induced cytoskeletal stabilization, brought about by phosphorylation of cofilin. Cofilin plays an important role in actin depolymerization, a process required for the changes in cell shape during migration. Phosphorylation of cofilin renders it unable to depolymerize F-actin, thereby stabilizing the cytoskeleton. Using immunostaining for phosphorylated cofilin (p-cofilin), we demonstrate that SPNs in wild-type animals, but not in reeler mutants and other mutants of the Reelin signalling cascade, are immunoreactive for p-cofilin. These findings suggest that Reelin near the central canal induces cofilin phosphorylation in SPNs, thereby preventing them from aberrant migration towards the central canal. The results extend our previous studies on cortical neurons in which Reelin in the marginal zone was found to stabilize the leading processes of migrating neurons and terminate the migration process.

KW - Animals

KW - Mice

KW - Mice, Knockout

KW - Staining and Labeling methods

KW - histology

KW - Phosphorylation

KW - Neurons cytology

KW - Mice, Neurologic Mutants

KW - Receptors, LDL genetics

KW - Cell Adhesion Molecules, Neuronal genetics

KW - Extracellular Matrix Proteins genetics

KW - Nerve Tissue Proteins genetics

KW - Serine Endopeptidases genetics

KW - Actin Depolymerizing Factors genetics

KW - Autonomic Fibers, Preganglionic metabolism

KW - Ganglia, Sympathetic cytology

KW - Spinal Cord anatomy

KW - Animals

KW - Mice

KW - Mice, Knockout

KW - Staining and Labeling methods

KW - histology

KW - Phosphorylation

KW - Neurons cytology

KW - Mice, Neurologic Mutants

KW - Receptors, LDL genetics

KW - Cell Adhesion Molecules, Neuronal genetics

KW - Extracellular Matrix Proteins genetics

KW - Nerve Tissue Proteins genetics

KW - Serine Endopeptidases genetics

KW - Actin Depolymerizing Factors genetics

KW - Autonomic Fibers, Preganglionic metabolism

KW - Ganglia, Sympathetic cytology

KW - Spinal Cord anatomy

M3 - SCORING: Zeitschriftenaufsatz

VL - 32

SP - 1611

EP - 1617

JO - EUR J NEUROSCI

JF - EUR J NEUROSCI

SN - 0953-816X

IS - 10

M1 - 10

ER -