Abstract
The vimentin network displays remarkable plasticity to support basic cellular functions. Here, we show that in several cell types vimentin filaments redistribute to the cell periphery during mitosis, forming a robust scaffold interwoven with cortical actin. Importantly, the intrinsically disordered tail domain of vimentin is essential for this redistribution, which allows normal mitotic progression. A tailless vimentin mutant forms curly bundles, which remain entangled with dividing chromosomes in mitosis leading to mitotic catastrophes or asymmetric partitions. Serial deletions of the tail domain induce an increasing impairment of cortical association and mitosis progression. Disruption of actin, but not microtubules, mimics the impact of tail deletion. Pathophysiological stimuli, including HIV-protease and lipoxidation, induce similar alterations. Interestingly, filament integrity is not necessary for cortical association, which also occurs in vimentin particles. Taken together, these results unveil novel implications of vimentin dynamics in cell division, in which the tail domain plays a key role.
