RT Journal Article
SR Electronic
T1 Vimentin filaments interact with the mitotic cortex allowing normal cell division
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 356642
DO 10.1101/356642
A1 Sofia Duarte
A1 Álvaro Viedma-Poyatos
A1 Elena Navarro-Carrasco
A1 Alma E. Martínez
A1 María A. Pajares
A1 Dolores Pérez-Sala
YR 2018
UL http://biorxiv.org/content/early/2018/06/27/356642.abstract
AB 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.