RT Journal Article
SR Electronic
T1 Material aging causes centrosome weakening and disassembly during mitotic exit
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 866434
DO 10.1101/866434
A1 Matthäus Mittasch
A1 Vanna M. Tran
A1 Manolo U. Rios
A1 Anatol W. Fritsch
A1 Stephen J. Enos
A1 Beatriz Ferreira Gomes
A1 Alec Bond
A1 Moritz Kreysing
A1 Jeffrey B. Woodruff
YR 2019
UL http://biorxiv.org/content/early/2019/12/05/866434.abstract
AB Centrosomes must resist microtubule-mediated forces for mitotic chromosome segregation. During mitotic exit, however, centrosomes are deformed and fractured by those same forces, which is a key step in centrosome disassembly. How the functional material properties of centrosomes change throughout the cell cycle, and how they are molecularly tuned remain unknown. Here, we used optically-induced flow perturbations to determine the molecular basis of centrosome strength and ductility in C. elegans embryos. We found that both properties declined sharply at anaphase onset, long before natural disassembly. This mechanical transition required PP2A phosphatase and correlated with inactivation of PLK-1 (Polo Kinase) and SPD-2 (Cep192). In vitro, PLK-1 and SPD-2 directly protected centrosome scaffolds from force-induced disassembly. Our results suggest that, prior to anaphase, PLK-1 and SPD-2 confer strength and ductility to the centrosome scaffold so that it can resist microtubule-pulling forces. In anaphase, centrosomes lose PLK-1 and SPD-2 and transition to a weak, brittle state that enables force-mediated centrosome disassembly.