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. 2023 Jun 29;55(7):1149–1163. doi: 10.1038/s41588-023-01424-9

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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 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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Extended Data Fig. 5 — (a) Schematic of the orthologous Fam5^snv variant introduced into mouse. (b-e) Immunofluorescent staining for ISL1 (blue) and GATA2 (red) on cross sections from WT (b,c) and Fam5^snv/snv (d,e) E14.5 hindbrains at r4 (b,d) and r6 (c,e) levels. Development of ISL1^ON;GATA2^ON IEEs was similar in WT (dashed region in b; inset) and Fam5^snv/snv (dashed region in d; inset) embryos, as was the formation of the facial motor nucleus (dotted regions in c,e). n = 4 (b,c), 4 (d,e) embryos. Scale bar = 200μm in (b) and applies to (b-e). (f) Generation of a humanized cRE1 duplication model. Tandem copies of human cRE1 (yellow arrows, (hg19 chr3:128,175,708-128,176,563) were inserted between the endogenous murine cRE1 and cRE2 loci.