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. 2017 Aug 9;7:7703. doi: 10.1038/s41598-017-08140-5

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Activation of phosphatidyl inositol-3 kinase (PI3K) rescues migration defects. (a) Coronal sections of P4 brains electroporated at E15 with shIGF-1R/CAG-GFP, control shRNA/CAG-GFP or shIGF-1R/CAG-GFP together with a constitutively active form of PI3K (p110CAAX-right); Calibration bar = 100 μm. (b) Quantification of the distribution of GFP-positive cells in VZ/SVZ/IZ, and layers II-IV and V-VI as indicated in (a). Note the significant increase in GFP positive cells in the deep layers (VZ/SVZ/IZ) zones and the decrease of GFP positive cells in the upper layers (II-IV) when knocking down IGF-1R. Co-transfection with p110CAAX rescued migration defects Post hoc Turkey’s ANOVA **p ≤ 0.01, ***p ≤ 0,0001. n = 3 independent experiments. An average of 500 cells was scored for each condition.