Semaphorin-3A guides radial migration of cortical neurons during development

2007 ◽  
Vol 11 (1) ◽  
pp. 36-44 ◽  
Author(s):  
Gang Chen ◽  
Jian Sima ◽  
Ming Jin ◽  
Kai-yu Wang ◽  
Xiao-jing Xue ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Semaphorin 3A ◽  
Radial Migration

scholarly journals BMP signaling and radial migration of cortical neurons

2017 ◽  
Vol 145 ◽  
pp. S115
Author(s):  
Nitin Agnihotri ◽  
Monika Saxena ◽  
Jonaki Sen
Keyword(s):  
Cortical Neurons ◽  
Bmp Signaling ◽  
Radial Migration

Cellular migration patterns in the developing mouse cerebral cortex

Development ◽  
1990 ◽  
Vol 110 (3) ◽  
pp. 713-732 ◽  
Author(s):  
C.P. Austin ◽  
C.L. Cepko
Keyword(s):  
Cortical Neurons ◽  
Intermediate Zone ◽  
Cellular Migration ◽  
Three Dimensions ◽  
Cortical Plate ◽  
Cortical Cells ◽  
Migration Patterns ◽  
Embryonic Mouse ◽  
Radial Migration ◽  
Almost All

The migration patterns of embryonic mouse cortical cells were investigated using a replication-incompetent retrovirus vector (BAG). The lateral ventricles of embryonic day 12 mouse embryos were infected with BAG and brains were harvested 2, 3, 4 and 6 days after infection. The location and morphology of all infected cortical cells were recorded from serial sections of entire brains, which were then reconstructed in three dimensions. Examination of the distribution of labelled cells revealed that there were migration patterns characteristic of each medial-lateral domain of the cortex. In the medial and dorsal areas, migration was often radial, although tangential spread increased with survival time, in large part due to ramification of cells in the intermediate zone. In the dorsolateral and lateral areas of the cortex, radial migration was generally not observed. Rather, variable extents of tangential migration occurred, and often resulted in wide separation of cells in the cortical plate. Almost all of the cellular dispersion occurred in the intermediate zone, although a modest degree of dispersion also occurred within the cortical plate itself. Most dispersion occurred in the mediolateral plane, with relatively little dispersion along the anteroposterior axis. Though characteristic migration patterns could be defined, wide variability in the extents of radial migration and tangential separation of cells was seen. The patterns of migration paralleled the distribution of radial glial fibers in all areas, and are most likely a reflection of the role of this network in supporting the migration of cortical neurons. The extent and variability of cellular dispersion supports a lineage-independent mechanism of cortical column ontogenesis.

scholarly journals Involvement of the Phosphatidylinositol 3-Kinase/Rac1 and Cdc42 Pathways in Radial Migration of Cortical Neurons

2004 ◽  
Vol 280 (6) ◽  
pp. 5082-5088 ◽  
Author(s):  
Daijiro Konno ◽  
Saori Yoshimura ◽  
Kei Hori ◽  
Hisato Maruoka ◽  
Kenji Sobue
Keyword(s):  
Cortical Neurons ◽  
Phosphatidylinositol 3 Kinase ◽  
Radial Migration ◽  
Phosphatidylinositol 3

scholarly journals Loss of BAF Complex in Developing Cortex Perturbs Radial Neuronal Migration in a WNT Signaling-Dependent Manner

2021 ◽  
Vol 14 ◽  
Author(s):  
Godwin Sokpor ◽  
Cemil Kerimoglu ◽  
Huong Nguyen ◽  
Linh Pham ◽  
Joachim Rosenbusch ◽  
...  
Keyword(s):  
Gene Expression ◽  
Wnt Signaling ◽  
Neuronal Migration ◽  
Cortical Neurons ◽  
Gene Expression Program ◽  
Dependent Manner ◽  
Related Factors ◽  
Baf Complex ◽  
Radial Migration ◽  
Expression Program

Radial neuronal migration is a key neurodevelopmental event indispensable for proper cortical laminar organization. Cortical neurons mainly use glial fiber guides, cell adhesion dynamics, and cytoskeletal remodeling, among other discrete processes, to radially trek from their birthplace to final layer positions. Dysregulated radial migration can engender cortical mis-lamination, leading to neurodevelopmental disorders. Epigenetic factors, including chromatin remodelers have emerged as formidable regulators of corticogenesis. Notably, the chromatin remodeler BAF complex has been shown to regulate several aspects of cortical histogenesis. Nonetheless, our understanding of how BAF complex regulates neuronal migration is limited. Here, we report that BAF complex is required for neuron migration during cortical development. Ablation of BAF complex in the developing mouse cortex caused alteration in the cortical gene expression program, leading to loss of radial migration-related factors critical for proper cortical layer formation. Of note, BAF complex inactivation in cortex caused defective neuronal polarization resulting in diminished multipolar-to-bipolar transition and eventual disruption of radial migration of cortical neurons. The abnormal radial migration and cortical mis-lamination can be partly rescued by downregulating WNT signaling hyperactivity in the BAF complex mutant cortex. By implication, the BAF complex modulates WNT signaling to establish the gene expression program required for glial fiber-dependent neuronal migration, and cortical lamination. Overall, BAF complex has been identified to be crucial for cortical morphogenesis through instructing multiple aspects of radial neuronal migration in a WNT signaling-dependent manner.

scholarly journals GSK-3 signaling in developing cortical neurons is essential for radial migration and dendritic orientation

eLife ◽  
2014 ◽  
Vol 3 ◽  
Author(s):  
Meghan Morgan-Smith ◽  
Yaohong Wu ◽  
Xiaoqin Zhu ◽  
Julia Pringle ◽  
William D Snider
Keyword(s):  
Signaling Pathways ◽  
Cortical Neurons ◽  
Apical Dendrite ◽  
Regulatory Proteins ◽  
Radial Migration ◽  
Tangential Migration ◽  
Mouse Mutants ◽  
Basal Dendrites ◽  
Dendritic Arbors ◽  
Gsk 3Β

GSK-3 is an essential mediator of several signaling pathways that regulate cortical development. We therefore created conditional mouse mutants lacking both GSK-3α and GSK-3β in newly born cortical excitatory neurons. Gsk3-deleted neurons expressing upper layer markers exhibited striking migration failure in all areas of the cortex. Radial migration in hippocampus was similarly affected. In contrast, tangential migration was not grossly impaired after Gsk3 deletion in interneuron precursors. Gsk3-deleted neurons extended axons and developed dendritic arbors. However, the apical dendrite was frequently branched while basal dendrites exhibited abnormal orientation. GSK-3 regulation of migration in neurons was independent of Wnt/β-catenin signaling. Importantly, phosphorylation of the migration mediator, DCX, at ser327, and phosphorylation of the semaphorin signaling mediator, CRMP-2, at Thr514 were markedly decreased. Our data demonstrate that GSK-3 signaling is essential for radial migration and dendritic orientation and suggest that GSK-3 mediates these effects by phosphorylating key microtubule regulatory proteins.

scholarly journals Dynein activating adaptor BICD2 controls radial migration of upper-layer cortical neurons in vivo

2019 ◽  
Vol 7 (1) ◽  
Author(s):  
Lena Will ◽  
Sybren Portegies ◽  
Jasper van Schelt ◽  
Merel van Luyk ◽  
Dick Jaarsma ◽  
...  
Keyword(s):  
Cortical Neuron ◽  
Cortical Neurons ◽  
Cortical Development ◽  
Adaptor Protein ◽  
Cortical Plate ◽  
Neuron Migration ◽  
Knock Out ◽  
Radial Migration

Abstract For the proper organization of the six-layered mammalian neocortex it is required that neurons migrate radially from their place of birth towards their designated destination. The molecular machinery underlying this neuronal migration is still poorly understood. The dynein-adaptor protein BICD2 is associated with a spectrum of human neurological diseases, including malformations of cortical development. Previous studies have shown that knockdown of BICD2 interferes with interkinetic nuclear migration in radial glial progenitor cells, and that Bicd2-deficient mice display an altered laminar organization of the cerebellum and the neocortex. However, the precise in vivo role of BICD2 in neocortical development remains unclear. By comparing cell-type specific conditional Bicd2 knock-out mice, we found that radial migration in the cortex predominantly depends on BICD2 function in post-mitotic neurons. Neuron-specific Bicd2 cKO mice showed severely impaired radial migration of late-born upper-layer neurons. BICD2 depletion in cortical neurons interfered with proper Golgi organization, and neuronal maturation and survival of cortical plate neurons. Single-neuron labeling revealed a specific role of BICD2 in bipolar locomotion. Rescue experiments with wildtype and disease-related mutant BICD2 constructs revealed that a point-mutation in the RAB6/RANBP2-binding-domain, associated with cortical malformation in patients, fails to restore proper cortical neuron migration. Together, these findings demonstrate a novel, cell-intrinsic role of BICD2 in cortical neuron migration in vivo and provide new insights into BICD2-dependent dynein-mediated functions during cortical development.

scholarly journals Nitric Oxide Synthase 1 Adaptor Protein, a Protein Implicated in Schizophrenia, Controls Radial Migration of Cortical Neurons

2015 ◽  
Vol 77 (11) ◽  
pp. 969-978 ◽  
Author(s):  
Damien Carrel ◽  
Kristina Hernandez ◽  
Munjin Kwon ◽  
Christine Mau ◽  
Meera P. Trivedi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Cortical Neurons ◽  
Protein A ◽  
Adaptor Protein ◽  
Radial Migration ◽  
Nitric Oxide Synthase 1 ◽  
Oxide Synthase

scholarly journals Synapsin III Acts Downstream of Semaphorin 3A/CDK5 Signaling to Regulate Radial Migration and Orientation of Pyramidal Neurons In Vivo

Cell Reports ◽  
2015 ◽  
Vol 11 (2) ◽  
pp. 234-248 ◽  
Author(s):  
Laura E. Perlini ◽  
Joanna Szczurkowska ◽  
Bryan A. Ballif ◽  
Alessandra Piccini ◽  
Silvio Sacchetti ◽  
...  
Keyword(s):  
Pyramidal Neurons ◽  
Semaphorin 3A ◽  
Radial Migration ◽  
Synapsin Iii
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