RT Journal Article
SR Electronic
T1 Mechanosensitive control of mitotic entry
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 2021.09.23.461473
DO 10.1101/2021.09.23.461473
A1 Margarida Dantas
A1 Andreia Oliveira
A1 Paulo Aguiar
A1 Helder Maiato
A1 Jorge G. Ferreira
YR 2022
UL http://biorxiv.org/content/early/2022/03/02/2021.09.23.461473.abstract
AB As cells prepare to divide, they must ensure that enough space is available to assemble the mitotic machinery without perturbing tissue homeostasis1. To do so, cells undergo a series of biochemical reactions regulated by cyclin B1-CDK1 that trigger the reorganization of the actomyosin cytoskeleton2 and ensure the coordination of cytoplasmic and nuclear events3.Along with the biochemical events that control mitotic entry, mechanical forces have recently emerged as important players in the regulation of cell cycle events4–6. However, the exact link between mechanical forces and the biochemical pathways that control mitotic progression remains to be established. Here, we identify a mechanical signal on the nucleus that helps set the time for nuclear envelope permeabilization (NEP) and mitotic entry. This signal relies on actomyosin contractility, which leads to nuclear unfolding during the G2-M transition, activating the stretch-sensitive cPLA2 on the nuclear envelope. This contributes to the spatiotemporal translocation of cyclin B1 to the nucleus. Our data demonstrate how nuclear mechanics during the G2-M transition contribute to timely and efficient mitotic spindle assembly and prevents chromosomal instability.Competing Interest StatementThe authors have declared no competing interest.