Unconventional myosin that functions as actin-based motor protein with ATPase activity (By similarity). Plays a role in the formation of Kupffer's vesicle, an organ that functions as left-right organizer during embryogenesis (PubMed:29769531, PubMed:30139971). Plays a role in vesicular trafficking events that are required for normal lumen expansion of Kupffer's vesicle (PubMed:30139971). Required for normal orientation of cilia in Kupffer's vesicle, and thus for normal, unidirectional circular flow and normal angular flow velocity, which then mediates asymmetric gene expression and left-right asymmetric development (PubMed:29769531). Plays a role in endosomal protein trafficking, and especially in the transfer of cargo proteins from early to recycling endosomes (By similarity). Required for normal planar cell polarity in ciliated cells, for normal rotational polarity of cilia, and for coordinated, unidirectional ciliary movement (By similarity). Interacts (via the two IQ motifs) with calmodulin. Interacts with F-actin. Colocalizes with the actin cytoskeleton in the cell cortex close to the apical cell membrane. Colocalizes with cytoplasmic puncta that are reminiscent of transport vesicles. Expressed both maternally and zygotically (PubMed:29769531). Ubiquitous in embryos at the four cell stage (PubMed:30139971). Detected at the eight cell stage. Detected at low levels throughout the embryo at the six somite stage, with higher levels in the developing notochord (PubMed:29769531). Binds a calmodulin chain via each of the two IQ domains. IQ domain 1 mediates interaction with calmodulin both in the presence and in the absence of Ca(2+). IQ domain 2 mediates interaction with calmodulin in the presence of Ca(2+). The TH1 domain is required for activity in complementing zebrafish defects in Kupffer's vesicle lumen size. Morpholino knockdown of the protein causes situs inversus, a left-right asymmetry defect where organs are placed at a position corresponding to the mirror image of the normal body plan. Causes laterality defects at the level of the heart, viscera and brain (PubMed:29769531). Morpholino knockdown of the protein leads to the formation of a Kupffer's vesicle with reduced volume and dismorphic shape. Morpholino knockdown of the protein interferes with the normal cellular remodeling that gives rise to anterior-posterior asymmetry of Kupffer's vesicle. Cells with a columnar shape persist at the posterior end of the vesicle, contrary to wild-type, where cells display columnar shape at the anterior part of the vesicle, and squamous or cuboidal shape at the posterior end of Kupffer's vesicle. Epithelial cells lining Kupffer's vesicle display an increased number of vacuoles, and disruption of the normal, directed vacuolar trafficking toward the apical cell membrane (PubMed:30139971). Agents that activate cftr increase the size of Kupffer's vesicle in myo1d mutants (PubMed:29769531, PubMed:30139971). Expansion of the lumen size is not sufficient to restore the normal spherical shape of Kupffer's vesicle and rescue laterality defects (PubMed:29769531, PubMed:30139971). Heterologous expression of rat Myo1d can complement the defects in Kupffer's vesicle lumen size and anterior-posterior cell shape changes (PubMed:30139971). Belongs to the TRAFAC class myosin-kinesin ATPase superfamily. Myosin family. Represents an unconventional myosin that should not be confused with the conventional myosin-1. Another kind of harmony - Issue 213 of April 2019