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. 2023 Apr 12;616(7957):495–503. doi: 10.1038/s41586-023-05868-1

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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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Extended Data Fig. 12 — a. ChIP-seq experiment in mouse embryonic branchial arches performed in Amin et al. 2015, which shows the binding profile of HoxA2 to Gli3 genomic locus. b. Whole-mount in situ hybridization of gli3 in zebrafish embryos inyected with a hoxd13a-GR mRNA. Developing fins are indicated with red arrowheads. In the absence of dexamethasone (left panel), the construct is inactive and the embryos develop normally (50 out of 57, 88%). Upon treatment with dexamethasone (right panel), hoxd13a is activated and causes a reduction of gli3 expression at the developing fin region (mild reduction in 39 out of 93, 42%; strong reduction in 22 out of 93, 24%). Scale bars = 250 µm.