FoxP2 protein levels regulate cell morphology changes and migration patterns in the vertebrate developing telencephalon
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In the mammalian telencephalon, part of the progenitor cells transition from multipolar to bipolar morphology as they invade the mantle zone. This associates with changing patterns of radial migration. However, the molecules implicated in these morphology transitions are not well known. In the present work, we analyzed the function of FoxP2 protein in this process during telencephalic development in vertebrates. We analyzed the expression of FoxP2 protein and its relation with cell morphology and migratory patterns in mouse and chicken developing striatum. We observed FoxP2 protein expressed in a gradient from the subventricular zone to the mantle layer in mice embryos. In the FoxP2 low domain cells showed multipolar migration. In the striatal mantle layer where FoxP2 protein expression is higher, cells showed locomoting migration and bipolar morphology. In contrast, FoxP2 showed a high and homogenous expression pattern in chicken striatum, thus bipolar morphology predominated. Elevation of FoxP2 in the striatal subventricular zone by in utero electroporation promoted bipolar morphology and impaired multipolar radial migration. In mouse cerebral cortex we obtained similar results. FoxP2 promotes transition from multipolar to bipolar morphology by means of gradiental expression in mouse striatum and cortex. Together these results indicate a role of FoxP2 differential expression in cell morphology control of the vertebrate telencephalon.
KeywordsRadial migration Bipolar morphology Striatum Cortex
We thank gratefully P. Almagro and J.E. Martínez-López for the technical support. We thank Dr. MA Nieto for the pCX-GFP plasmid. This work was supported by Spanish Ministry of Science and Innovation Grant BFU-2011-27326, Institute of Health Carlos III, Spanish Cell Therapy Network and Research Center of Mental Health (RD06/0010/0023; RD12/0019/0024), General Council of Valencia (Prometeo 2009/028 and 11/2011/042). E.G.C. was supported by the Postdoctoral Program of the “Consejo Superior de Investigaciones Científicas-Junta de Ampliación de Estudios.”