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. 2023 May 10;617(7960):325–334. doi: 10.1038/s41586-023-05895-y

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© The Author(s) 2023

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — a, Number of putative IGC events intersecting exons of protein-coding genes as a function of a gene’s pLI. Of the 799 genes, 314 (39.3%) did not have a pLI score and are shown in the column labelled No pLI data available. b,c, Number of times a gene exon acts as an acceptor (b) or a donor (c) of an IGC event. d,e, IGC events at the complement factor locus, C4A and C4B (d), and the opsin middle- and long-wavelength-sensitive genes associated with colour blindness (OPN1MW and OPN1LW locus; e). Predicted donor (orange) and acceptor (blue) segments by length (number to left of event) and average number of supporting SNVs (number to right of event) are shown. The number of human haplotypes supporting each configuration is depicted by the histograms to the right. f,g, IGC events that reposition entire gene models for the FCGR (f) and TRIM (g) loci.