Fig. 1: Myo1G regulates heart and brain LR asymmetry independent of the LRO flow.
From: Myosin1G promotes Nodal signaling to control zebrafish left-right asymmetry
a, a′ Quantification of cardiac jogging indicates that MZ myo1g mutants present laterality defects that are enhanced in MZ myo1d; MZ myo1g double mutants (a). Concomitant inactivation of the LRO flow (through dnaaf1 mutation) reveals that MZ myo1d/g mutations enhance the cardiac jogging defects of flow-deficient animals (a′). b Brain asymmetry is impaired in MZ myo1g single and MZ myo1d; MZ myo1g double mutants. Frontal views of pitx2 expression at 30 somites, dorsal up. c MZ myo1g mutants do not show visceral LR defects. L liver, G gut, P pancreas. Dorsal views of foxa1 expression at 48 h, anterior up. d MZ myo1d/g inactivation enhances the brain laterality phenotypes of LRO flow-deficient dnaaf1 mutants. e, f Visceral laterality phenotypes of dnaaf1 mutants are unaffected by myo1d/g inactivation. f Dorsal views of foxa1 expression at 48 h, anterior up. Pictures are derived from the data set quantified in (e). Scale bars: 50 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.
