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Polarized endosome dynamics by spindle asymmetry during asymmetric cell division

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During asymmetric division, fate determinants at the cell cortex segregate unequally into the two daughter cells. It has recently been shown that Sara signaling endosomes in the cytoplasm also segregate asymmetrically during asymmetric division. Biased dispatch of Sara endosomes mediates asymmetric Notch/Delta signaling during the asymmetric division of Sensory Organ Precursors (SOP) in Drosophila. In flies, this has been generalized to stem cells in the gut and the central nervous system and, in zebrafish, to neural precursors of the spinal cord. However, the mechanism of asymmetric endosome segregation is not known. Here we unravelled this mechanism. The plus-end kinesin motor Klp98A targets Sara endosomes to the central spindle. At the central spindle, endosomes move bidirectionally on an antiparallel array of microtubules. The microtubule depolymerising kinesin Klp10A and its antagonist Patronin generate central spindle asymmetry. The asymmetric spindle, in turn, polarizes endosome motility, ultimately causing asymmetric endosome dispatch into one daughter cell. To demonstrate this, we inverted the polarity of the spindle by polar targeting of Patronin using nanobodies. Spindle inversion targets the endosomes to the wrong cell. To explain quantitatively how spindle asymmetry controls endosomes asymmetry, we developed a theory of the motility of endosomes in an asymmetric microtubule antiparallel overlap. This theory defines a very simple equation explaining quantitatively this complex cellular behavior. Our data uncovers the molecular and physical mechanism by which organelles localized away from the cellular cortex can be dispatched asymmetrically during asymmetric division. Moreover, our theory can readily be applied beyond asymmetric division to explain polarized traffic in other microtubule antiparallel overlaps, for instance in vertebrate dendrites.

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