Abstract
The proper structural organization of the microtubule-based spindle during cell division requires the activity of non-motor microtubule-associated proteins, which crosslink microtubules to regulate filament sliding rates and assemble microtubule arrays. PRC1 is an essential MAP that preferentially crosslinks overlapping antiparallel microtubules at the spindle midzone. PRC1 has been proposed to act as a molecular brake, but insight into the mechanism of how PRC1 molecules function cooperatively to resist motor-driven microtubule sliding and to allow for the formation of stable midzone overlaps has been lacking.
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