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. 2018 Nov 21;8:17201. doi: 10.1038/s41598-018-35506-0

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© The Author(s) 2018

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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Examples of CNVs detected by SNP-based CMA. (A) Copy number analysis identified a chromosome 17q terminal gain not detectable with conventional karyotyping in the SiPSC line “CT1-S1-010”. (B) FISH analysis showing the unbalanced translocation 14p/17q in this clone (left = metaphase, right = interphase). (C) Conventional karyotyping and copy number analysis of chromosome 9 of the SiPSC line “i82A-S1-004” revealed unremarkable results (Log2Ratio top), but SNP allele peak distribution (xAllelePeaks bottom) uncovered a copy neutral allelic imbalance on the long arm of chromosome 9 (4 bands) while the short arm (left) shows normal allelic distribution (3 bands) (see also Fig. S2). (D) Two independent overlapping intragenic deletions in the CTNNA3 gene detected in the RiPSC lines “i88H-R1-001” (green bottom) and “iO3H-R1-001” (blue bottom) and absent from their fibroblast cultures “f88H-X-001” (green top) and “iO3H-X-001” (blue top).