Microtubule-sliding modules based on kinesins EG5 and PRC1-dependent KIF4A drive human spindle elongation

• DOI: 10.1016/j.devcel.2021.04.005
• Publication Date: 2021-04-27T16:14:03Z
• Authors: Kruno Vukušić; Ivana Ponjavić; Renata Buđa; Patrik Risteski; Iva M. Tolić
• Keywords: Kinesin

Proper chromosome segregation into two future daughter cells requires the mitotic spindle to elongate in anaphase. However, although some candidate proteins are implicated this process, molecular mechanism that drives elongation human is unknown. Using combined depletion and inactivation assays together with CRISPR technology explore redundancy between multiple targets, we discovered force-generating of consists EG5/kinesin-5 PRC1-dependent motor KIF4A/kinesin-4, contribution from kinesin-6 kinesin-8. Disruption EG5 KIF4A leads total failure due blocked elongation, despite poleward motion. Tubulin photoactivation, stimulated emission (STED), expansion microscopy show perturbation both impairs midzone microtubule sliding without affecting stability. Thus, mechanistically distinct modules, one based on a self-sustained other crosslinker-assisted motor, power cells.