Fig. 2

MZ myosin1g mutants display impaired Nodal signaling. a MZ myo1g single and MZ myo1d; MZ myo1g double mutants fail to display asymmetric lft2 expression in the cardiac primordium. Dorsal views at 22 somites, anterior up. b–d MZ myo1d/g mutants display a reduced anterior propagation of the expression of the Nodal ligand spaw (b, see also Supplementary Fig. 3a), the Nodal effector pitx2 (c, see also Supplementary Fig. 3b) and the Nodal feedback inhibitor lft1 (d). Lateral views at 18 somites, anterior left, dorsal up. Box plots in (b–d) indicate mean values ± SD. e Left-sided expression of Spaw RNA partially rescues the cardiac jogging defects of MZ myo1g mutants (see also Supplementary Fig. 4a, b). f Enhancing Spaw signaling through furinA RNA injection similarly rescues the cardiac jogging defects of MZ myo1g mutants. Scale bars: a 50 µm, b–d 100 µm. All p values were obtained using non-directional statistical tests. Complete numerical and statistical information for all experiments are provided in the Source Data files.