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. 2018 Jul 2;8:9966. doi: 10.1038/s41598-018-27767-6

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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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Induction of the T315I mutation in TCCS and KOPM28. (a) Efficiencies in establishment of imatinib-resistant sublines. The vertical axis indicates percentage (%) establishment of imatinib-resistant sublines, and the horizontal axis indicates days after imatinib selection. Efficiencies in SCR7-treated TCCS (red) and KOPM28 (blue) electroporated with reverse sgRNA and anti-sense ccODN are indicated. (b) Electrophoresis of PCR products after EcoRI digestion. Upper and lower panels indicate parental cells and imatinib-resistant sublines of TCCS and KOPM28, respectively. Full-length gels are presented in Supplementary Figs S2 and S3. (c,d) Sequences of PCR products. Sequences of parental cells and three imatinib-sublines of TCCS (c) and KOPM28 (d) are indicated. Wild-type genomic and amino acid sequences and mutations in template sequence for HR are indicated at the top of the panel. Arrowheads in each sequence indicate mutations as a result of HR-mediated gene editing.