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. 2017 Sep 18;8:578. doi: 10.1038/s41467-017-00654-w

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© The Author(s) 2017

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. 5 — Deletion of Vegfr3 fails to rescue coronary defects in Pofut1 ^cKO or Dll4 ^cKO mice. a PECAM1 staining and IB4/SMMHC co-staining shows increased coronaries in E16.5 heart with endocardial Pofut1 deletion, which cannot be rescued by simultaneous deletion of Vegfr3. IB4 and SMMHC co-staining shows defective major coronary arteries (arrowhead) remain in the double mutants. b PECAM1 staining shows increased coronaries in E15.5 Dll4 ^cKO heart by induced Dll4 deletion at E14.5, which cannot be rescued by simultaneous deletion of Vegfr3. PECAM1/DLL4 or VEGFR2/VEGFR3 co-staining shows effective deletion of Dll4 or Vegfr3