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. 2018 Jun 28;9:2526. doi: 10.1038/s41467-018-04931-0

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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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Fig. 5 — Association of hESC-CM promoter interactions with cardiac conduction and rhythm disorders. a QQ plots of –log₁₀(p values) corresponding to SNPs located in the top 20% cPIR or hESC PIRs of three GWAS studies, congenital heart disease^{25, 26} (CHD; total SNPs = 500K; hESC-CM SNPs = 19K; hESC SNPs = 19K), coronary artery disease²⁶ (CAD; total SNPs = 9.5 M; hESC-CM SNPs = 289K; hESC SNPs = 328K; http://www.cardiogramplusc4d.org) and cardiac conduction and rhythm disorders²⁷ (CRD; total SNPs = 2.5 M; hESC-CM SNPs =85K; hESC SNPs = 80K), against randomised PIRs (average of 1000 permutations). Significance of overlaps between GWAS SNPs (p < 0.001) and the top 20% cPIRs or hESC PIRs were tested using GoShifter²⁸. b Manhattan plot of CRD GWAS²⁷. Green spots indicate inflated SNPs in the cPIR/randomised PIR QQ plot with p < 0.001. Red gene names are nearest genes to the SNPs in the significant peaks assigned by the GWAS and black gene names are target genes interacting with the cPIRs containing the significant SNPs (p < 1 × 10⁻⁵)