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. 2019 May 30;125(2):170–183. doi: 10.1161/CIRCRESAHA.118.314515

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© 2019 The Authors.

Circulation Research is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial-NoDerivs License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited, the use is noncommercial, and no modifications or adaptations are made.

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Figure 3. — Loss of SRSF3 (serine/arginine splicing factor 3) in the developing heart results in embryonically lethal heart defects. A and B, Hematoxylin and eosin (H&E) staining in sections of αMHC-Cre embryos (A) and SRSF3-floxed/αMHC-Cre embryos (B) at E9.5. The boxed areas in A and B are shown at high magnification in A′ and B′, illustrating the cell deficit in the developing ventricular wall of SRSF3-floxed/αMHC-Cre embryos. Bar, 250 µm (A and B), 50 μm (A′ and B′). C and D, Immunofluorescence analysis in sections of αMHC-Cre embryos (C) and SRSF3-floxed/αMHC-Cre embryos (D) at E10.5, using anti-phospho-Histone H3 (red), anti-TroponinT (green), and Dapi (blue). Arrows indicate cardiomyocytes positive for phospho-histone H3; the developing SRSF3-floxed/αMHC-Cre heart is devoid of these cells. Bar, 20 μm.