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Neuron. 2015 Jul 15;87(2):311-25. doi: 10.1016/j.neuron.2015.06.023.

Bcl11a (Ctip1) Controls Migration of Cortical Projection Neurons through Regulation of Sema3c.

Author information

1
Institute of Molecular and Cellular Anatomy, Ulm University, Albert-Einstein-Allee 11, 89081 Ulm, Germany.
2
Max Delbrück Center for Molecular Medicine, Robert-Rössle-Strasse 10, 13125 Berlin, Germany.
3
Institute of Cell Biology and Neurobiology, Center for Anatomy, Charité-Universitätsmedizin Berlin, Virchowweg 6, 10117 Berlin, Germany.
4
Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1HH, UK.
5
The Methodist Hospital Research Institute, 6670 Bertner Avenue, Houston, TX 77030, USA.
6
Institute of Cell Biology and Neurobiology, Center for Anatomy, Charité-Universitätsmedizin Berlin, Virchowweg 6, 10117 Berlin, Germany; Institute of Biology and Biomedicine, Lobachevsky State University of Nizhny Novgerod, 23 Prospekt Gagarina (Gagarin Avenue), 603950 Nizhny Novgorod, Russia.
7
Institute of Molecular and Cellular Anatomy, Ulm University, Albert-Einstein-Allee 11, 89081 Ulm, Germany. Electronic address: stefan.britsch@uni-ulm.de.

Abstract

During neocortical development, neurons undergo polarization, oriented migration, and layer-type-specific differentiation. The transcriptional programs underlying these processes are not completely understood. Here, we show that the transcription factor Bcl11a regulates polarity and migration of upper layer neurons. Bcl11a-deficient late-born neurons fail to correctly switch from multipolar to bipolar morphology, resulting in impaired radial migration. We show that the expression of Sema3c is increased in migrating Bcl11a-deficient neurons and that Bcl11a is a direct negative regulator of Sema3c transcription. In vivo gain-of-function and rescue experiments demonstrate that Sema3c is a major downstream effector of Bcl11a required for the cell polarity switch and for the migration of upper layer neurons. Our data uncover a novel Bcl11a/Sema3c-dependent regulatory pathway used by migrating cortical neurons.

PMID:
26182416
DOI:
10.1016/j.neuron.2015.06.023
[Indexed for MEDLINE]
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