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Background    Nkx2.7  is the  tinman -related gene, as well as orthologs of  Nkx2.5  and  Nkx-2.3 . Nkx2.7 and Nkx2.5 express in zebrafish heart fields of lateral plate mesoderm. The temporal and spatial expression patterns of  Nkx2.7  are similar to those of  Nkx2.5 , but their functions during cardiogenesis remain unclear.    Methodology/Principal Findings  Here, Nkx2.7 is demonstrated to compensate for Nkx2.5 loss of function and play a predominant role in the lateral development of the heart, including normal cardiac looping and chamber formation. Knocking down Nkx2.5 showed that heart development was normal from 24 to 72 hpf. However, when knocking down either Nkx2.7 or Nkx2.5 together with Nkx2.7, it appeared that the heart failed to undergo looping and showed defective chambers, although embryos developed normally before the early heart tube stage. Decreased ventricular myocardium proliferation and defective myocardial differentiation appeared to result from late-stage up-regulation of  bmp4 ,  versican ,  tbx5  and  tbx20 , which were all expressed normally in hearts at an early stage. We also found that  tbx5  and  tbx20  were modulated by  Nkx2.7  through the heart maturation stage because an inducible overexpression of  Nkx2.7  in the heart caused down-regulation of  tbx5  and  tbx20 . Although heart defects were induced by overexpression of an injection of 150-pg  Nkx2.5  or 5-pg  Nkx2.7  mRNA, either  Nkx2.5  or  Nkx2.7  mRNA rescued the defects induced by Nkx2.7-morpholino(MO) and Nkx2.5-MO with Nkx2.7-MO.    Conclusions and Significance  Therefore, we conclude that redundant activities of Nkx2.5 and Nkx2.7 are required for cardiac morphogenesis, but that Nkx2.7 plays a more critical function, specifically indicated by the gain-of-function and loss-of- function experiments where  Nkx2.7  is observed to regulate the expressions of  tbx5  and  tbx20  through the maturation stage.

Nkx2.7 and Nkx2.5 Function Redundantly and Are Required for Cardiac Morphogenesis of Zebrafish Embryos