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. 2018 Mar 9;8:4277. doi: 10.1038/s41598-018-22753-4

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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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Identification of noncanonical imprinting in the PFC of the offspring without and with ASD and editing of KMT2C transcript in human PFC. (a) Sanger sequencing was used to analyze noncanonical imprinting of NOS1 in the PFC of the offspring without and with ASD. “M*” stands for maternally-biased expression. (b) Schematic diagram of the genomic locus of human KMT2C. Arrows indicate the direction of transcription. (c) Sanger sequencing was performed to analyze RNA editing for KMT2C in the PFC of the offspring without and with ASD, fetal PFC, and blood from parents of the fetus. (d) Schematic diagram of the genomic locus of mouse Kmt2c. Arrows indicate the direction of transcription. (e) Sanger sequencing was performed to analyze RNA editing for Kmt2c in PFC and blood from postnatal day 28 (P28) mice and PFC from embryonic day 15.5 (E15.5) mice. SNP information is shown as (paternal allele/maternal allele).