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. 2011 Oct 15;138(20):4499–4509. doi: 10.1242/dev.067454

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© 2011.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial Share Alike License (http://creativecommons.org/licenses/by-nc-sa/3.0), which permits unrestricted non-commercial use, distribution and reproduction in any medium provided that the original work is properly cited and all further distributions of the work or adaptation are subject to the same Creative Commons License terms.

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Fig. 3. — Npnt knockdown causes extension of the AV canal. (A-D) Projections of confocal images of hearts from control (A,C) and MO2-injected (B,D) embryos from transgenic Tg(myl7:EGFP-HsHRAS)^s883 (A,B) and Tg(–5.1myl7:nDsRed2)f2 (C,D) zebrafish at 52 hpf, suggesting an extension of the AV canal (brackets) in npnt morphants. (E) Representative images of hearts from control, MO2-injected and MO2 + npnt mRNA-injected embryos from transgenic Tg(myl7:EGFP-HsHRAS)^s883 zebrafish at 52 hpf. Brackets indicate the AV boundary. (F) Quantitative analysis (n>160 from three independent experiments; mean ± s.e.m.). Note that injection of npnt mRNA rescued the MO2-mediated AV canal extension. (G) Quantitative analysis scoring of type I (mild extension of the AV canal), type II (obvious extension of the AV canal) and type III (straight heart) AV canal defects (mean ± s.e.m.). A, atrium; V, ventricle. Scale bars: 50 μm.