Reply to: Zebrafish prrx1a mutants have normal hearts

[No abstract; first paragraph shown] In our original paper we showed that left–right (L–R) asymmetric cell movements towards the midline produced differential forces that lead to a leftward displacement of the cardiac posterior pole, initiating heart laterality1. We also showed that the cell movements were mediated by the L–R asymmetric activation (higher on the right) of transcription factors (Snail and/or Prrx) that induce epithelial–mesenchymal transition (EMT), and that this cellular behaviour is conserved in zebrafish, chicken and mouse1. In the accompanying Comment, Tessadori et al.2 question the role of Prrx1a in heart laterality in zebrafish, after generating mutants that do not present heart laterality defects. Injection of one of the morpholinos we used (MO1) into zygotic prrx1ael558 and prrx1ahu13685 mutant embryos led to a cardiac phenotype that was considered to result from off-target mediated effects that act early in development and alter the structure of the left–right organizer (LRO) (also known as Kupffer’s vesicle) in zebrafish3,4,5. Thus, two questions arise. First, whether the mesocardia phenotype that we observed in prrx1a-MO1 embryos was due to non-specific off-target effects; and second, whether Prrx1a is dispensable for heart laterality in zebrafish. Here we provide new data indicating that Prrx1a has a role in heart laterality in zebrafish (Fig. 1).