Myosin1G promotes Nodal signaling to control Zebrafish Left-Right asymmetry

Abstract Myosin1D (Myo1D) has recently emerged as a conserved regulator of animal LR asymmetry that governs the morphogenesis of the central LR Organizer (LRO). In addition to Myo1D, the zebrafish genome encodes the closely related Myo1G. While Myo1G also controls LR asymmetry, we show that it does so through an entirely different mechanism. Myo1G promotes the Nodal-mediated transfer of laterality information from the LRO to target tissues.