A radial glia-specific role of RhoA in double cortex formation

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

A radial glia-specific role of RhoA in double cortex formation. / Cappello, Silvia; Böhringer, Christian R J; Bergami, Matteo; Conzelmann, Karl-Klaus; Ghanem, Alexander; Tomassy, Giulio Srubek; Arlotta, Paola; Mainardi, Marco; Allegra, Manuela; Caleo, Matteo; van Hengel, Jolanda; Brakebusch, Cord; Götz, Magdalena.

In: Neuron, Vol. 73, No. 5, 08.03.2012, p. 911-24.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Cappello, S, Böhringer, CRJ, Bergami, M, Conzelmann, K-K, Ghanem, A, Tomassy, GS, Arlotta, P, Mainardi, M, Allegra, M, Caleo, M, van Hengel, J, Brakebusch, C & Götz, M 2012, 'A radial glia-specific role of RhoA in double cortex formation', Neuron, vol. 73, no. 5, pp. 911-24. https://doi.org/10.1016/j.neuron.2011.12.030

APA

Cappello, S., Böhringer, C. R. J., Bergami, M., Conzelmann, K-K., Ghanem, A., Tomassy, G. S., Arlotta, P., Mainardi, M., Allegra, M., Caleo, M., van Hengel, J., Brakebusch, C., & Götz, M. (2012). A radial glia-specific role of RhoA in double cortex formation. Neuron, 73(5), 911-24. https://doi.org/10.1016/j.neuron.2011.12.030

Vancouver

Cappello S, Böhringer CRJ, Bergami M, Conzelmann K-K, Ghanem A, Tomassy GS et al. A radial glia-specific role of RhoA in double cortex formation. Neuron. 2012 Mar 8;73(5):911-24. https://doi.org/10.1016/j.neuron.2011.12.030

Author

Cappello, Silvia ; Böhringer, Christian R J ; Bergami, Matteo ; Conzelmann, Karl-Klaus ; Ghanem, Alexander ; Tomassy, Giulio Srubek ; Arlotta, Paola ; Mainardi, Marco ; Allegra, Manuela ; Caleo, Matteo ; van Hengel, Jolanda ; Brakebusch, Cord ; Götz, Magdalena. / A radial glia-specific role of RhoA in double cortex formation. In: Neuron. 2012 ; Vol. 73, No. 5. pp. 911-24.

Bibtex

@article{0b2d73349f464b51be91df3e6aa02289,

title = "A radial glia-specific role of RhoA in double cortex formation",

abstract = "The positioning of neurons in the cerebral cortex is of crucial importance for its function as highlighted by the severe consequences of migrational disorders in patients. Here we show that genetic deletion of the small GTPase RhoA in the developing cerebral cortex results in two migrational disorders: subcortical band heterotopia (SBH), a heterotopic cortex underlying the normotopic cortex, and cobblestone lissencephaly, in which neurons protrude beyond layer I at the pial surface of the brain. Surprisingly, RhoA(-/-) neurons migrated normally when transplanted into wild-type cerebral cortex, whereas the converse was not the case. Alterations in the radial glia scaffold are demonstrated to cause these migrational defects through destabilization of both the actin and the microtubules cytoskeleton. These data not only demonstrate that RhoA is largely dispensable for migration in neurons but also showed that defects in radial glial cells, rather than neurons, can be sufficient to produce SBH.",

keywords = "Age Factors, Animals, Animals, Newborn, Bromodeoxyuridine, Cell Movement, Cell Proliferation, Cerebral Cortex, Classical Lissencephalies and Subcortical Band Heterotopias, Disease Models, Animal, Electroporation, Embryo, Mammalian, Embryonic Stem Cells, Female, GAP-43 Protein, Gene Expression Regulation, Developmental, Green Fluorescent Proteins, Mice, Mice, Transgenic, Nerve Tissue Proteins, Neuroglia, Neurons, Pregnancy, Silver Staining, rhoA GTP-Binding Protein",

author = "Silvia Cappello and B{\"o}hringer, {Christian R J} and Matteo Bergami and Karl-Klaus Conzelmann and Alexander Ghanem and Tomassy, {Giulio Srubek} and Paola Arlotta and Marco Mainardi and Manuela Allegra and Matteo Caleo and {van Hengel}, Jolanda and Cord Brakebusch and Magdalena G{\"o}tz",

year = "2012",

month = mar,

day = "8",

doi = "10.1016/j.neuron.2011.12.030",

language = "English",

volume = "73",

pages = "911--24",

journal = "Neuron",

issn = "0896-6273",

publisher = "Cell Press",

number = "5",

}

RIS

TY - JOUR

T1 - A radial glia-specific role of RhoA in double cortex formation

AU - Cappello, Silvia

AU - Böhringer, Christian R J

AU - Bergami, Matteo

AU - Conzelmann, Karl-Klaus

AU - Ghanem, Alexander

AU - Tomassy, Giulio Srubek

AU - Arlotta, Paola

AU - Mainardi, Marco

AU - Allegra, Manuela

AU - Caleo, Matteo

AU - van Hengel, Jolanda

AU - Brakebusch, Cord

AU - Götz, Magdalena

PY - 2012/3/8

Y1 - 2012/3/8

N2 - The positioning of neurons in the cerebral cortex is of crucial importance for its function as highlighted by the severe consequences of migrational disorders in patients. Here we show that genetic deletion of the small GTPase RhoA in the developing cerebral cortex results in two migrational disorders: subcortical band heterotopia (SBH), a heterotopic cortex underlying the normotopic cortex, and cobblestone lissencephaly, in which neurons protrude beyond layer I at the pial surface of the brain. Surprisingly, RhoA(-/-) neurons migrated normally when transplanted into wild-type cerebral cortex, whereas the converse was not the case. Alterations in the radial glia scaffold are demonstrated to cause these migrational defects through destabilization of both the actin and the microtubules cytoskeleton. These data not only demonstrate that RhoA is largely dispensable for migration in neurons but also showed that defects in radial glial cells, rather than neurons, can be sufficient to produce SBH.

AB - The positioning of neurons in the cerebral cortex is of crucial importance for its function as highlighted by the severe consequences of migrational disorders in patients. Here we show that genetic deletion of the small GTPase RhoA in the developing cerebral cortex results in two migrational disorders: subcortical band heterotopia (SBH), a heterotopic cortex underlying the normotopic cortex, and cobblestone lissencephaly, in which neurons protrude beyond layer I at the pial surface of the brain. Surprisingly, RhoA(-/-) neurons migrated normally when transplanted into wild-type cerebral cortex, whereas the converse was not the case. Alterations in the radial glia scaffold are demonstrated to cause these migrational defects through destabilization of both the actin and the microtubules cytoskeleton. These data not only demonstrate that RhoA is largely dispensable for migration in neurons but also showed that defects in radial glial cells, rather than neurons, can be sufficient to produce SBH.

KW - Age Factors

KW - Animals

KW - Animals, Newborn

KW - Bromodeoxyuridine

KW - Cell Movement

KW - Cell Proliferation

KW - Cerebral Cortex

KW - Classical Lissencephalies and Subcortical Band Heterotopias

KW - Disease Models, Animal

KW - Electroporation

KW - Embryo, Mammalian

KW - Embryonic Stem Cells

KW - Female

KW - GAP-43 Protein

KW - Gene Expression Regulation, Developmental

KW - Green Fluorescent Proteins

KW - Mice

KW - Mice, Transgenic

KW - Nerve Tissue Proteins

KW - Neuroglia

KW - Neurons

KW - Pregnancy

KW - Silver Staining

KW - rhoA GTP-Binding Protein

U2 - 10.1016/j.neuron.2011.12.030

DO - 10.1016/j.neuron.2011.12.030

M3 - Journal article

C2 - 22405202

VL - 73

SP - 911

EP - 924

JO - Neuron

JF - Neuron

SN - 0896-6273

IS - 5

ER -

ID: 40299471