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. 2018 Aug 20;8:12420. doi: 10.1038/s41598-018-30436-3

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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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Production and genotyping of gene-edited Guangxi Bama minipigs. (A) A total of nine cloned piglets from three litters appeared healthy at birth. (B) BmgBI digestion analysis showed that eight of nine piglets were monoallelic mutant at the SCNA locus (labeled by red asterisks), and the remaining one (1–4#) was a wild-type (WT). WT minipig were used as a negative control and the repair vector as a positive control. (C) Genotype-confirmed mutant minipigs (labeled by red asterisks) and the one wild-type minipig remained clinically healthy and showed normal growth and development at 3 months of age. (D) One mutant minipig (1–2#) and the age-matched wild type (1–4#) were used to confirm the SCNA mutations at the transcriptional level. The SCNA mRNA-coding sequence was obtained by RT-PCR. (E) The presence of the desired mutations at the transcriptional level (sequence coding for SCNA mRNA) was confirmed by DNA sequencing.

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