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. 2019 Nov 12;7:277. doi: 10.3389/fcell.2019.00277

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Copyright © 2019 Xue, Liu, Wen, Yang, Gao, Tao and Zhou.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Aberrant activation of Mef2c due to the disruption of Vgll4b-Mef2c complex, accounts for the valvulogenesis defects in vgll4b mutants. (A–C) Mef2cb mRNA was injected into one-cell stage wild type embryos. (D–G) Mef2cb DN, mef2cb DN R3T, and mef2cb-sumo1 mRNA rescue assays in vgll4b^–/– embryos. (H) Schematic representation of variant forms of Mef2cb, including WT, DN, R3T, and Sumo1 fusion mutants. (I–L) Cmlc2:mef2cb DN or flk1:mef2cb DN plasmid rescue assays in vgll4b^–/– embryos. (M–P) Representative images show Alcam staining of sibling and vgll4b^–/– embryos rescued with cmlc2:mef2cb DN or flk1:mef2cb DN plasmid at 52 hpf. The endocardial cushion cells expressing Alcam were indicated by asterisks. Scale bar: 10 μm.