Impairment of radial glial scaffold-dependent neuronal migration and formation of double cortex by genetic ablation of afadin

Yamamoto, Hideaki; Mandai, Kenji; Konno, Daijiro; Maruo, Tomohiko; Matsuzaki, Fumio; Takai, Yoshimi

doi:10.1016/j.brainres.2015.05.012

Cited by 24 publications

(19 citation statements)

References 56 publications

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“…In addition to the previously described roles of Afadin in cell proliferation and adherens junction maintenance in cortical development [12, 18], our findings provide new evidence that Afadin regulates mitotic division orientation of radial glial cells. The developing Afadin mutant cortices were characterized by increased numbers of obliquely-oriented cell divisions in the VZ.…”

Section: Discussionsupporting

confidence: 79%

“…Previous studies using Emx1-Cre ( Emx1-Cre; Mllt4 fl/fl mice) showed that conditional deletion of Afadin from developing cortical radial glial cells at E9.5 resulted in hyperproliferation and radial glial disorganization [12, 18]. To examine in detail the cellular and tissue architecture regulated by Afadin in cortical development, we first characterized the distribution of proteins found in adherens and tight junctions in cortical progenitors using the same Emx1-Cre; Mllt4 fl/fl mice.…”

Section: Resultsmentioning

confidence: 99%

“…In Mllt4 knockout brains (right panel), random diffusion of AJ and apicobasal polarity-associated proteins is allowed, disrupting cell division orientation and triggering progenitor delamination, and premature fate determination. Disruption of the radial glial scaffold [18] allows random dispersion throughout the cortical wall VZ: ventricular zone; SVZ: subventricular zone; CP: cortical plate …”

Section: Discussionmentioning

confidence: 99%

“…Knockout mouse studies showed that Afadin is essential for cell adhesion, polarization, differentiation, and migration in the very early embryo [17]. More recently, Afadin was found to be highly expressed in VZ progenitor cells [18], and conditional deletion of Afadin from the cortical neuroepithelium resulted in loss of adherens junctions, increased proliferation, and abnormalities in radial glial morphology [12, 18]. Whether loss of Afadin led to changes in VZ cell polarity and mitotic orientation was not described.…”

Section: Introductionmentioning

confidence: 99%

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Afadin controls cell polarization and mitotic spindle orientation in developing cortical radial glia

et al. 2017

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BackgroundIn developing tissues, cell polarity and tissue architecture play essential roles in the regulation of proliferation and differentiation. During cerebral cortical development, adherens junctions link highly polarized radial glial cells in a neurogenic niche that controls their behavior. How adherens junctions regulate radial glial cell polarity and/or differentiation in mammalian cortical development is poorly understood.ResultsConditional deletion of Afadin, a protein required for formation and maintenance of epithelial tissues, leads to abnormalities in radial glial cell polarity and subsequent loss of adherens junctions. We observed increased numbers of obliquely-oriented progenitor cell divisions, increased exit from the ventricular zone neuroepithelium, and increased production of intermediate progenitors.ConclusionsTogether, these findings indicate that Afadin plays an essential role in regulating apical-basal polarity and adherens junction integrity of radial glial cells, and suggest that epithelial architecture plays an important role in radial glial identity by regulating mitotic orientation and preventing premature exit from the neurogenic niche.Electronic supplementary materialThe online version of this article (doi:10.1186/s13064-017-0085-2) contains supplementary material, which is available to authorized users.

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Section: Discussionsupporting

confidence: 79%

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Afadin controls cell polarization and mitotic spindle orientation in developing cortical radial glia

et al. 2017

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“…The nectin-afadin system maintains the formation of AJs between RGCs in the midbrain and the dorsal telencephalon and between ependymal cells in the midbrain in concert with N-cadherin for the formation of the layer structure in the developing cerebral cortex (Gil-Sanz et al 2014;Yamamoto et al 2013Yamamoto et al , 2015. In the midbrain, loss of afadin causes hydrocephalus by mislocalization of RGCs in the ventricular and intermediate zones, mislocalization of neurons at the surface of the cerebral aqueduct, and loss of ependymal cells from the ventricular and aqueductal surfaces, accompanied by the reduced localization of nectin-1 and N-cadherin and the disruption of AJs.…”

Section: Hydrocephalus and Subcortical Band Heterotopiamentioning

confidence: 99%

Cooperative Roles of Nectins with Cadherins in Physiological and Pathological Processes

Fujiwara

Mizoguchi

Takai

2016

The Cadherin Superfamily

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Mammalian tissues and organs are composed of cells of different types and these cells adhere to one another to form societies of cells including the mesenchyme and the epithelium. Cell-cell adhesion in the mesenchyme is weak whereas cells are organized into closely adherent barrier-forming sheets by cellcell adhesions in the epithelium. Cell-cell adhesion is organized to allow the release or incorporation of individual cells during various physiological or pathological processes, for example, organ development and growth, maintenance and repair of tissues, or tumorigenesis. One prominent cell-cell adhesion apparatus is adherens junctions (AJs). The central structural components of AJs are transmembrane cellcell adhesion molecules, cadherins and nectins. Nectins recruit cadherins to the cell-cell contact sites and mediate cell-cell adhesions that control local membrane dynamics for cell polarization and coordinate shape change at the cellular level. Nectins are engaged in calcium-independent homophilic and heterophilic transinteractions between opposing cells in numerous tissues and cell types to form homotypic and heterotypic cell-cell adhesion, whereas cadherins are primarily involved in calcium-dependent homophilic trans-interactions between opposing cells to form homotypic cell-cell adhesion. Nectins function cooperatively with or independently of cadherins to control physiological processes and cooperative ones include the formation of AJs and apico-basal polarity, apical constriction, contact inhibition of cell movement and proliferation, formation of synapse, formation of checkerboard-like cell arrangement, ciliary epithelium and lens, and

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Being a Neural Stem Cell: A Matter of Character But Defined by the Microenvironment

Andreopoulou

Arampatzis

Patsoni

et al. 2017

Advances in Experimental Medicine and Biology

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The cells that build the nervous system, either this is a small network of ganglia or a complicated primate brain, are called neural stem and progenitor cells. Even though the very primitive and the very recent neural stem cells (NSCs) share common basic characteristics that are hard-wired within their character, such as the expression of transcription factors of the SoxB family, their capacity to give rise to extremely different neural tissues depends significantly on instructions from the microenvironment. In this chapter we explore the nature of the NSC microenvironment, looking through evolution, embryonic development, maturity and even disease. Experimental work undertaken over the last 20 years has revealed exciting insight into the NSC microcosmos. NSCs are very capable in producing their own extracellular matrix and in regulating their behaviour in an autocrine and paracrine manner. Nevertheless, accumulating evidence indicates an important role for the vasculature, especially within the NSC niches of the postnatal brain; while novel results reveal direct links between the metabolic state of the organism and the function of NSCs.

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Impairment of radial glial scaffold-dependent neuronal migration and formation of double cortex by genetic ablation of afadin

Cited by 24 publications

References 56 publications

Afadin controls cell polarization and mitotic spindle orientation in developing cortical radial glia

Afadin controls cell polarization and mitotic spindle orientation in developing cortical radial glia

Cooperative Roles of Nectins with Cadherins in Physiological and Pathological Processes

Being a Neural Stem Cell: A Matter of Character But Defined by the Microenvironment

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