Myo1G regulates heart and brain LR asymmetry independent of the LRO flow. 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.
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