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. 2020 Nov 19;11:88. doi: 10.1186/s13229-020-00387-6

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© The Author(s) 2020

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — Symmetric copy number variations at 7q11.23. a Schematic representation of genotype–phenotype correlation in WBS and 7Dup patients, compared to healthy control (CTL), indicating opposite and shared phenotypes. Genomic organization of WBS region with the 17 genes that are significantly expressed in neurons, in bold the four genes selected for their critical role in the pathogenesis of both WBS and 7Dup. b Lentiviral vector (top) and PiggyBac-based construct (bottom) used to induce iPSC differentiation into cortical neurons. Ubc: human Ubiquitin constitutive promoter, rtTA: TET transactivator promoter gene, NGN2: Neurogenin2 gene, Puro^R: Puromycin resistance gene, Bsd^R: Blasticidin resistance gene, white triangles represent terminal repeats of the transposon