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. 2018 Jan 25;9:368. doi: 10.1038/s41467-017-02796-3

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© The Author(s) 2018

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. 1 — Compact myocardium development is disrupted with endothelial-specific knockout of Ino80. a Quantitative PCR analysis of endothelial cells (ECs) isolated from control (Ctrl) and Tie2Cre;Ino80 fl/fl (CKO) hearts reveal that Vegfr2 is expressed while Ino80 mRNA is undetectable. Error bars in graphs are standard deviation. (control, n = 3 hearts; mutant, n = 3 hearts). b Measurements of the area covered by compact myocardium in tissue sections from control or Tie2Cre;Ino80 fl/fl hearts at the indicated embryonic stages. NS nonsignificant, *P < 0.05; **P < 0.01, evaluated by Student’s t-test. c, d Tissue sections stained with Hematoxylin and Eosin show trabecular myocardium (TM) and compact myocardium (CM) in control (c) and CKO hearts (d). Images are representative of the following number of replicates: control, n = 6 hearts; mutant, n = 5 hearts at e12.5, control, n = 9 hearts; mutant, n = 6 hearts at e15.5. Scale bars: 100 μm. e Compact myocardium (orange brackets) is not thin with myocardial-specific deletion of Ino80 (Myh6Cre;Ino80 fl/fl). Images are representative of the following number of replicates: control, n = 6 hearts; mutant, n = 5 hearts. Scale bars: 100 μm. f Trabecular myocardium thickness is increased in the left and right ventricles in Ino80 CKOs. Error bars in graphs are sd. (control, n = 6 hearts; mutant, n = 5 hearts at e12.5, control, n = 9 hearts; mutant, n = 6 hearts at e15.5). ***P < 0.001; ****P < 0.0001, evaluated by Student’s t-test. g The normal growth in compact layer thickness from e12.5 to 15.5 is replaced by an abnormal expansion of the trabecular layer in mutant hearts. Error bars in graphs are standard deviation. (control, n = 6 hearts; mutant, n = 5 hearts at e12.5, control, n = 9 hearts; mutant, n = 6 hearts at e15.5). NS nonsignificant, **P < 0.01; ****P < 0.0001, evaluated by Student’s t-test. h Endomucin (EMCN) immunofluorescence to label endocardium shows an expansion of this cell type into the area occupied by compact myocardium in control hearts. Images are representative of the following number of replicates: n = 9 hearts; mutant, n = 6 hearts at e15.5. Scale bars: 100 μm