Sema3E/PlexinD1 regulates the migration of hem-derived Cajal-Retzius cells in developing cerebral cortex

Ana Bribián, Sara Nocentini, Franc Llorens, Vanessa Gil, Erik Mire, Diego Reginensi, Yutaka Yoshida, Fanny Mann and José Antonio del Río ()
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Ana Bribián: Molecular and Cellular Neurobiotechnology, Institute of Bioengineering of Catalonia (IBEC), Parc Científic de Barcelona
Sara Nocentini: Molecular and Cellular Neurobiotechnology, Institute of Bioengineering of Catalonia (IBEC), Parc Científic de Barcelona
Franc Llorens: Molecular and Cellular Neurobiotechnology, Institute of Bioengineering of Catalonia (IBEC), Parc Científic de Barcelona
Vanessa Gil: Molecular and Cellular Neurobiotechnology, Institute of Bioengineering of Catalonia (IBEC), Parc Científic de Barcelona
Erik Mire: Developmental Biology, Institute of Marseille Luminy, CNRS UMR 6216, University of the Mediterranean, Parc Scientifique de Luminy
Diego Reginensi: Molecular and Cellular Neurobiotechnology, Institute of Bioengineering of Catalonia (IBEC), Parc Científic de Barcelona
Yutaka Yoshida: Cincinnati Children’s Hospital Medical Center
Fanny Mann: Developmental Biology, Institute of Marseille Luminy, CNRS UMR 6216, University of the Mediterranean, Parc Scientifique de Luminy
José Antonio del Río: Molecular and Cellular Neurobiotechnology, Institute of Bioengineering of Catalonia (IBEC), Parc Científic de Barcelona

Nature Communications, 2014, vol. 5, issue 1, 1-14

Abstract: Abstract During the development of the cerebral cortex, Cajal-Retzius (CR) cells settle in the preplate and coordinate the precise growth of the neocortex. Indeed, CR cells migrate tangentially from specific proliferative regions of the telencephalon (for example, the cortical hem (CH)) to populate the entire cortical surface. This is a very finely tuned process regulated by an emerging number of factors that has been sequentially revealed in recent years. However, the putative participation of one of the major families of axon guidance molecules in this process, the Semaphorins, was not explored. Here we show that Semaphorin-3E (Sema3E) is a natural negative regulator of the migration of PlexinD1-positive CR cells originating in the CH. Our results also indicate that Sema3E/PlexinD1 signalling controls the motogenic potential of CR cells in vitro and in vivo. Indeed, absence of Sema3E/PlexinD1 signalling increased the migratory properties of CR cells. This modulation implies negative effects on CXCL12/CXCR4 signalling and increased ADF/Cofilin activity.

Date: 2014
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DOI: 10.1038/ncomms5265

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