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. 2017 Aug 8;7:7554. doi: 10.1038/s41598-017-06211-1

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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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Alternative splicing event in Bcas1, Sema6a and Capzb in QKI ^{FL/FL;Olig2-Cre} and QKI ^FL/FL;- mice. (a,b,c) Left: IGV views of the exon skipping events in Bcas1, Sema6a and Capzb. All samples are represented on the same scale for each screenshot. Black arrows represent the primers used for validation by RT-PCR. Right: Validation of exon skipping events by semi-quantitative PCR in n = 3 mice per genotype. The constitutive exon is present in all isoforms of the gene and is not alternatively spliced. The pixel densities of PCR bands from 3 independent mice brain RNA samples were quantified using ImageJ software, normalized over wild-type mice and represented as mean ± SEM (Student t-test, **p < 0.001).