β1 Integrins in Radial Glia But Not in Migrating Neurons Are Essential for the Formation of Cell Layers in the Cerebral Cortex

Belvindrah, Richard; Graus‐Porta, Diana; Goebbels, Sandra; Nave, Klaus Armin; Müller, Ulrich

doi:10.1523/jneurosci.4494-07.2007

Cited by 123 publications

(168 citation statements)

References 58 publications

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“…In agreement, the amount of phosphorylated focal adhesion kinase (pFAK) at T397, an active form of FAK, was decreased in Itgb1 f/f ; Emx1-Cre mice (Supplementary information, Figure S7), suggesting the inhibition of integrin-mediated focal adhesion signaling. Consistent with previous reports of restricted Itgb1 elimination in post-mitotic neurons [23,24], we found that both the cortex size and lamination were roughly normal in Itgb1 f/f ; Emx1-Cre or Itgb1 f/+ ; Emx1-Cre mice (Supplementary information, Figure S9). …”

Section: Itgb1 Is Required For Axon Formation In Cortical Neurons In supporting

confidence: 92%

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Laminin/β1 integrin signal triggers axon formation by promoting microtubule assembly and stabilization

et al. 2012

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Axon specification during neuronal polarization is closely associated with increased microtubule stabilization in one of the neurites of unpolarized neuron, but how this increased microtubule stability is achieved is unclear. Here, we show that extracellular matrix (ECM) component laminin promotes neuronal polarization via regulating directional microtubule assembly through β1 integrin (Itgb1). Contact with laminin coated on culture substrate or polystyrene beads was sufficient for axon specification of undifferentiated neurites in cultured hippocampal neurons and cortical slices. Active Itgb1 was found to be concentrated in laminin-contacting neurites. Axon formation was promoted and abolished by enhancing and attenuating Itgb1 signaling, respectively. Interestingly, laminin contact promoted plus-end microtubule assembly in a manner that required Itgb1. Moreover, stabilizing microtubules partially prevented polarization defects caused by Itgb1 downregulation. Finally, genetic ablation of Itgb1 in dorsal telencephalic progenitors caused deficits in axon development of cortical pyramidal neurons. Thus, laminin/Itgb1 signaling plays an instructive role in axon initiation and growth, both in vitro and in vivo, through the regulation of microtubule assembly. This study has established a linkage between an extrinsic factor and intrinsic cytoskeletal dynamics during neuronal polarization.

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Section: Itgb1 Is Required For Axon Formation In Cortical Neurons In supporting

confidence: 92%

“…npg adhesion molecules are involved in initial neuritogenesis [20], neurite outgrowth and regeneration [21], axon path finding [22], neuronal positioning [23][24][25], as well as synaptic development and plasticity [26]. However, whether and how integrin-mediated cell adhesion is involved in neuronal polarization is unknown.…”

Section: Wen-liang Lei Et Al 955mentioning

confidence: 99%

Laminin/β1 integrin signal triggers axon formation by promoting microtubule assembly and stabilization

et al. 2012

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“…A role for integrin ␤1 has also been demonstrated for the development of cortical and cerebellar radial glial cells, where it acts as an essential component of the endfeet anchorage to the external limiting membrane (Graus-Porta et al, 2001; Milner and Campbell, 2002;Belvindrah et al, 2007). We found that throughout development radial glial cells of the SCO express integrins ␣6 and ␤1, but not ␤3.…”

Section: Discussionsupporting

confidence: 66%

“…For instance, mice carrying mutations in integrin ␣6 and those lacking integrin ␤1 show defects in the anchorage of radial glial processes at the meningeal basement membrane in the cerebral and cerebellar cortex (Georges-Labouesse et al, 1998;Graus-Porta et al, 2001;Milner and Campbell, 2002;Belvindrah et al, 2007). On the other hand, integrins interact with the TSR domain of several members of the TSR superfamily (Leu et al, 2003;Calzada et al, 2004;Short et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Polarized expression of integrin β1 in diencephalic roof plate during chick development, a possible receptor for SCO‐spondin

Caprile

Osorio

Henríquez

et al. 2009

Developmental Dynamics

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The roof plate of the caudal diencephalon is formed by the posterior commissure (PC) and the underlying secretory ependyma, the subcommissural organ (SCO). The SCO is composed by radial glial cells bearing processes that cross the PC and attach to the meningeal basement membrane. Since early development, the SCO synthesizes SCO-spondin, a glycoprotein that shares similarities to axonal guidance proteins. In vitro, SCO-spondin promotes neuritic outgrowth through a mechanism mediated by integrin ␤1. However, the secretion of SCO-spondin toward the extracellular matrix that surrounds the PC axons and the expression of integrins throughout PC development have not been addressed. Here we provide immunohistochemical evidence to suggest that during chick development SCO cells secrete SCO-spondin through their basal domain, where it is deposited into the extracellular matrix in close contact with axons of the PC that express integrin ␤1. Our results suggest that SCO-spondin has a role in the development of the PC through its interaction with integrin ␤1.

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“…Cell-based assays implicate c-Src, PI3 kinase, and ERK1/2 in the CHL1-integrin signaling pathway [12]. Integrins have been shown to participate in the mechanism of radial migration of embryonic cortical neurons [13] but appear to function when expressed on radial glia, rather than on neurons [14]. Thus, a trans heterophilic interaction between CHL1 on neurons, and β1 integrins on radial glia, may transduce signaling in migrating cortical neurons responsible for correct laminar positioning.…”

Section: L1 and Chl1 As Signaling Co-receptors In Cortical Developmentmentioning

confidence: 99%

L1 and NCAM adhesion molecules as signaling coreceptors in neuronal migration and process outgrowth

Schmid

Maness

2008

Current Opinion in Neurobiology

202

169

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Summary of Recent AdvancesNeural cell adhesion molecules (CAMs) of the immunoglobulin superfamily engage in multiple neuronal interactions that influence cell migration, axonal and dendritic projection, and synaptic targeting. Their downstream signal transduction events specify whether a cell moves or projects axons and dendrites to targets in the brain. Many of the diverse functions of CAMs are brought about through homophilic and heterophilic interactions with other cell surface receptors. An emerging concept is that CAMs act as co-receptors to assist in intracellular signal transduction, and to provide cytoskeletal linkage necessary for cell and growth cone motility. Here we will focus on new discoveries that have revealed novel co-receptor functions for the best understood CAMs -L1, CHL1, and NCAM-important for neuronal migration and axon guidance. We will also discuss how dysregulation of CAMs may also bear on neuropsychiatric disease and cancer.

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β1 Integrins in Radial Glia But Not in Migrating Neurons Are Essential for the Formation of Cell Layers in the Cerebral Cortex

Cited by 123 publications

References 58 publications

Laminin/β1 integrin signal triggers axon formation by promoting microtubule assembly and stabilization

Laminin/β1 integrin signal triggers axon formation by promoting microtubule assembly and stabilization

Polarized expression of integrin β1 in diencephalic roof plate during chick development, a possible receptor for SCO‐spondin

L1 and NCAM adhesion molecules as signaling coreceptors in neuronal migration and process outgrowth

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