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. 2020 Apr 15;11:1845. doi: 10.1038/s41467-020-15598-x

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© The Author(s) 2020

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. 6 — a Schematics of the XPO5 allele design. b Loss of XPO5 results in embryonic lethality. XPO5 KO embryos show developmental defects as early as in E6.5 (c) and fails to go through gastrulation (d). Representative images of littermate embryos are shown for over ten control and KO embryos. e Whole-mount LacZ staining of XPO5^KI/+ (Ctrl) and XPO5^KI/KI (KO) shows universal expression of XPO5 throughout the embryo. f Depletion of XPO5 and mir-290 in XPO5 KO embryos at E7 is measured by qPCR. Dysregulation of selected genes in XPO5 KO embryos at E7 (g) and E8.5 (h) is measured by qPCR, respectively. Oct4 and Nanog are failed to be downregulated in XPO5 KO embryos at both E7 and E8.5. Scale bar 250 μm in c–e. Data shown are mean s.d. from three independent experiments. *P < 0.05; **P < 0.01; ***P < 0.001 determined by Student’s t test. Original data for f, g, and h are provided in the Source Data file.