Department of Cell and Systems Biology, University of Toronto, Toronto, Canada
Jessica Yu
Ted Rogers Centre for Heart Research, Translational Biology and Engineering Program, University of Toronto, Toronto, Canada; Institute of Biomaterials and Biomedical Engineering, University of Toronto, Toronto, Canada
Roman Korytnikov
Department of Cell and Systems Biology, University of Toronto, Toronto, Canada
Department of Cell and Systems Biology, University of Toronto, Toronto, Canada; Ted Rogers Centre for Heart Research, Translational Biology and Engineering Program, University of Toronto, Toronto, Canada; Institute of Biomaterials and Biomedical Engineering, University of Toronto, Toronto, Canada
In emerging epithelial tissues, cells undergo dramatic rearrangements to promote tissue shape changes. Dividing cells remain interconnected via transient cytokinetic bridges. Bridges are cleaved during abscission and currently, the consequences of disrupting abscission in developing epithelia are not well understood. We show that the Rab GTPase Rab25 localizes near cytokinetic midbodies and likely coordinates abscission through endomembrane trafficking in the epithelium of the zebrafish gastrula during epiboly. In maternal-zygotic Rab25a and Rab25b mutant embryos, morphogenic activity tears open persistent apical cytokinetic bridges that failed to undergo timely abscission. Cytokinesis defects result in anisotropic cell morphologies that are associated with a reduction of contractile actomyosin networks. This slows cell rearrangements and alters the viscoelastic responses of the tissue, all of which likely contribute to delayed epiboly. We present a model in which Rab25 trafficking coordinates cytokinetic bridge abscission and cortical actin density, impacting local cell shape changes and tissue-scale forces.
