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. 2022 Oct 13;14:119. doi: 10.1186/s13073-022-01118-7

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© The Author(s) 2022

Open AccessThis 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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — Description of WoL and distribution of lethal genes across these windows. Three-dimensional microCT images of wild-type mouse embryos corresponding to E9.5, E12.5, E15.5 and E18.5. The waffle chart shows the total number of lethal genes characterised through the secondary viability screening and their distribution by WoL. EL genes, where the embryo dies before E9.5 constitute nearly 50% of all the lethal genes in this dataset. This stage broadly correlates with the pre-organogenesis phase of embryonic development. Non-early lethal genes are divided into ML (17%) and LL (35%). The complete set of genes associated with each WoL is available in File S1 [33]. WoL, windows of lethality; E, embryonic day; EL, early gestation lethal; ML, mid gestation lethal; LL, late gestation lethal