How does Reelin control neuronal migration and layer formation in the developing mammalian neocortex?

Katsutoshi Sekine, Kenichiro Kubo, Kazunori Nakajima

Research output: Contribution to journalArticle

58 Citations (Scopus)

Abstract

The mammalian neocortex has a laminar structure that develops in a birth-date-dependent "inside-out" pattern. Its layered structure is established by neuronal migration accompanied by sequential changes in migratory mode regulated by several signaling cascades. Although Reelin was discovered about two decades ago and is one of the best known molecules that is indispensable to the establishment of the "inside-out" neuron layers, the cellular and molecular functions of Reelin in layer formation are still largely unknown. In this review article, we summarize our recent understanding of Reelin's functions during neuronal migration. Reelin acts in at least two different steps of neuronal migration: the final step of neuronal migration (somal/terminal translocation) just beneath the marginal zone (MZ) and the regulation of cell polarity step when the neurons change their migratory mode from multipolar migration to locomotion. During the translocation mode, Reelin activates integrin α5β1 through an intracellular pathway that triggers the translocation and activates N-cadherin in concert with the nectin-afadin system. Reelin is also involved in the termination of neuronal migration by degrading Dab1 via the SOCS7-Cullin5-Rbx2 system, and Reelin has been found to induce the birth-date-dependent neuronal aggregation in vivo. Based on these findings, we hypothesize that the molecular function of Reelin during neuronal migration is to control cell-adhesiveness during development by regulating the expression/activation of cell adhesion molecules.

Original languageEnglish
Pages (from-to)50-58
Number of pages9
JournalNeuroscience Research
Volume86
DOIs
Publication statusPublished - 2014 Sep 1

Fingerprint

Neocortex
Parturition
Neurons
Adhesiveness
Cell Polarity
Cell Adhesion Molecules
Cadherins
Locomotion
Integrins
nectins
afadin

Keywords

  • Cell adhesion molecules
  • Dab1
  • Inside-out
  • Primitive cortical zone
  • Reelin
  • Terminal translocation

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

How does Reelin control neuronal migration and layer formation in the developing mammalian neocortex? / Sekine, Katsutoshi; Kubo, Kenichiro; Nakajima, Kazunori.

In: Neuroscience Research, Vol. 86, 01.09.2014, p. 50-58.

Research output: Contribution to journalArticle

@article{6031375c62ff469cbc09ad944913beac,
title = "How does Reelin control neuronal migration and layer formation in the developing mammalian neocortex?",
abstract = "The mammalian neocortex has a laminar structure that develops in a birth-date-dependent {"}inside-out{"} pattern. Its layered structure is established by neuronal migration accompanied by sequential changes in migratory mode regulated by several signaling cascades. Although Reelin was discovered about two decades ago and is one of the best known molecules that is indispensable to the establishment of the {"}inside-out{"} neuron layers, the cellular and molecular functions of Reelin in layer formation are still largely unknown. In this review article, we summarize our recent understanding of Reelin's functions during neuronal migration. Reelin acts in at least two different steps of neuronal migration: the final step of neuronal migration (somal/terminal translocation) just beneath the marginal zone (MZ) and the regulation of cell polarity step when the neurons change their migratory mode from multipolar migration to locomotion. During the translocation mode, Reelin activates integrin α5β1 through an intracellular pathway that triggers the translocation and activates N-cadherin in concert with the nectin-afadin system. Reelin is also involved in the termination of neuronal migration by degrading Dab1 via the SOCS7-Cullin5-Rbx2 system, and Reelin has been found to induce the birth-date-dependent neuronal aggregation in vivo. Based on these findings, we hypothesize that the molecular function of Reelin during neuronal migration is to control cell-adhesiveness during development by regulating the expression/activation of cell adhesion molecules.",
keywords = "Cell adhesion molecules, Dab1, Inside-out, Primitive cortical zone, Reelin, Terminal translocation",
author = "Katsutoshi Sekine and Kenichiro Kubo and Kazunori Nakajima",
year = "2014",
month = "9",
day = "1",
doi = "10.1016/j.neures.2014.06.004",
language = "English",
volume = "86",
pages = "50--58",
journal = "Neuroscience Research",
issn = "0168-0102",
publisher = "Elsevier Ireland Ltd",

}

TY - JOUR

T1 - How does Reelin control neuronal migration and layer formation in the developing mammalian neocortex?

AU - Sekine, Katsutoshi

AU - Kubo, Kenichiro

AU - Nakajima, Kazunori

PY - 2014/9/1

Y1 - 2014/9/1

N2 - The mammalian neocortex has a laminar structure that develops in a birth-date-dependent "inside-out" pattern. Its layered structure is established by neuronal migration accompanied by sequential changes in migratory mode regulated by several signaling cascades. Although Reelin was discovered about two decades ago and is one of the best known molecules that is indispensable to the establishment of the "inside-out" neuron layers, the cellular and molecular functions of Reelin in layer formation are still largely unknown. In this review article, we summarize our recent understanding of Reelin's functions during neuronal migration. Reelin acts in at least two different steps of neuronal migration: the final step of neuronal migration (somal/terminal translocation) just beneath the marginal zone (MZ) and the regulation of cell polarity step when the neurons change their migratory mode from multipolar migration to locomotion. During the translocation mode, Reelin activates integrin α5β1 through an intracellular pathway that triggers the translocation and activates N-cadherin in concert with the nectin-afadin system. Reelin is also involved in the termination of neuronal migration by degrading Dab1 via the SOCS7-Cullin5-Rbx2 system, and Reelin has been found to induce the birth-date-dependent neuronal aggregation in vivo. Based on these findings, we hypothesize that the molecular function of Reelin during neuronal migration is to control cell-adhesiveness during development by regulating the expression/activation of cell adhesion molecules.

AB - The mammalian neocortex has a laminar structure that develops in a birth-date-dependent "inside-out" pattern. Its layered structure is established by neuronal migration accompanied by sequential changes in migratory mode regulated by several signaling cascades. Although Reelin was discovered about two decades ago and is one of the best known molecules that is indispensable to the establishment of the "inside-out" neuron layers, the cellular and molecular functions of Reelin in layer formation are still largely unknown. In this review article, we summarize our recent understanding of Reelin's functions during neuronal migration. Reelin acts in at least two different steps of neuronal migration: the final step of neuronal migration (somal/terminal translocation) just beneath the marginal zone (MZ) and the regulation of cell polarity step when the neurons change their migratory mode from multipolar migration to locomotion. During the translocation mode, Reelin activates integrin α5β1 through an intracellular pathway that triggers the translocation and activates N-cadherin in concert with the nectin-afadin system. Reelin is also involved in the termination of neuronal migration by degrading Dab1 via the SOCS7-Cullin5-Rbx2 system, and Reelin has been found to induce the birth-date-dependent neuronal aggregation in vivo. Based on these findings, we hypothesize that the molecular function of Reelin during neuronal migration is to control cell-adhesiveness during development by regulating the expression/activation of cell adhesion molecules.

KW - Cell adhesion molecules

KW - Dab1

KW - Inside-out

KW - Primitive cortical zone

KW - Reelin

KW - Terminal translocation

UR - http://www.scopus.com/inward/record.url?scp=84912535199&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84912535199&partnerID=8YFLogxK

U2 - 10.1016/j.neures.2014.06.004

DO - 10.1016/j.neures.2014.06.004

M3 - Article

VL - 86

SP - 50

EP - 58

JO - Neuroscience Research

JF - Neuroscience Research

SN - 0168-0102

ER -