ZFIN Image: Juan et al., 2018, Fig. 1

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Fig. 1

myo1D controls zebrafish left–right asymmetry. a Transgene-mediated expression of zebrafish myo1D (zmyo1D) restores the laterality of genitalia rotation in Drosophila myo1D (dmyo1D) mutant or dmyo1D RNAi flies. Lines 3 and 6 are two independent transgenic insertions. b–e Zebrafish MZ myo1D mutants present defects in leftward cardiac jogging. b–d Dorsal views of the cmlc2-expressing heart primordium at 26 hpf, anterior up. e Quantification of cardiac jogging defects in maternal (M) and maternal zygotic (MZ) myo1D^tj16b or myo1D^tj16c mutants. f–i Cardiac looping is affected in MZ myo1D mutants. f–h Frontal views of the cmlc2-expressing heart at 48 hpf, dorsal up. i Quantification of cardiac looping defects in M myo1D^tj16b and MZ myo1D^tj16b or MZ myo1D^tj16c mutants. j–m MZ myo1D mutants present defects in the leftward looping of the gut and the asymmetric development of the liver (black arrows) and pancreas (white arrows). j–l Dorsal views of foxa1-expressing visceral organs at 48 hpf, anterior up. n, o Overexpression of zebrafish myo1Cb RNA impairs cardiac jogging (n) and looping (o). MZ myo1G single mutants present laterality defects (n, o). MZ myo1D; MZ myo1G double mutants or MZ myo1D mutants injected with myo1Cb RNA present an increased frequency of defects compared to MZ myo1D mutants (n, o). Scale bars: 30 µm

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Acknowledgments

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