Emergence of asymmetry from an initially symmetrical state is a universal transition in Nature. Living organisms show striking asymmetries at the molecular, cellular, tissular and organismal level. However, whether and how multilevel asymmetries are related remains unclear. Here, we show that Drosophila Myosin 1D (Myo1D) and Myosin 1C (Myo1C) are sufficient to generate de novo directional twisting of cells, single organs or the whole body in opposite directions. We show that directionality lies in the Myosins’ motor domain and is swappable, and that Myo1D powers gliding of actin filaments in circular, counterclockwise paths in vitro. Altogether, our results reveal the molecular motor Myo1D as a chiral determinant, sufficient to break symmetry at all biological scales through chiral interaction with the actin cytoskeleton.

Left-right (LR) asymmetry is essential for organ development and function in metazoans, but how initial LR cue is relayed to tissues still remains unclear. Here, we propose a mechanism by which the Drosophila LR determinant Myosin ID (MyoID) transfers LR information to neighboring cells through the planar cell polarity (PCP) atypical cadherin Dachsous (Ds). Molecular interaction between MyoID and Ds in a specific LR organizer controls dextral cell polarity of adjoining hindgut progenitors and is required for organ looping in adults. Loss of Ds blocks hindgut tissue polarization and looping, indicating that Ds is a crucial factor for both LR cue transmission and asymmetric morphogenesis. We further show that the Ds/Fat and Frizzled PCP pathways are required for the spreading of LR asymmetry throughout the hindgut progenitor tissue. These results identify a direct functional coupling between the LR determinant MyoID and PCP, essential for non-autonomous propagation of early LR asymmetry.