1] Molecular and Cellular Neurobiotechnology, Institute of Bioengineering of Catalonia (IBEC), Parc Científic de Barcelona, E-08028 Barcelona, Spain [2] Department of Cell Biology, Universitat de Barcelona, E-08028 Barcelona, Spain [3] Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), E-08028 Barcelona, Spain [4].
1] Molecular and Cellular Neurobiotechnology, Institute of Bioengineering of Catalonia (IBEC), Parc Científic de Barcelona, E-08028 Barcelona, Spain [2] Department of Cell Biology, Universitat de Barcelona, E-08028 Barcelona, Spain [3] Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), E-08028 Barcelona, Spain.
Nat Commun. 2014 Jun 27;5:4265. doi: 10.1038/ncomms5265.
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.
在大脑皮层发育过程中，Cajal-Retzius（CR）细胞定位于基板，并协调新皮层的精确生长。事实上，CR 细胞从端脑的特定增殖区域（例如皮质半球（CH））沿切线迁移，以填充整个皮质表面。这是一个非常精细的调节过程，由近年来陆续揭示的越来越多的因素调控。然而，Semaphorin 家族的轴突导向分子之一在这个过程中的潜在参与，尚未得到探索。在这里，我们表明，Semaphorin-3E（Sema3E）是源自 CH 的 PlexinD1 阳性 CR 细胞迁移的天然负调节剂。我们的结果还表明，Sema3E/PlexinD1 信号控制 CR 细胞在体外和体内的运动潜能。事实上，缺乏 Sema3E/PlexinD1 信号会增加 CR 细胞的迁移特性。这种调节暗示对 CXCL12/CXCR4 信号的负影响和 ADF/Cofilin 活性的增加。
