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Regulated changes in material properties underlie centrosome disassembly during mitotic exit.

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Mittasch,  Matthäus
Max Planck Institute for Molecular Cell Biology and Genetics, Max Planck Society;

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Fritsch,  Anatol
Max Planck Institute for Molecular Cell Biology and Genetics, Max Planck Society;

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Gomes,  Beatriz Ferreira
Max Planck Institute for Molecular Cell Biology and Genetics, Max Planck Society;

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Kreysing,  Moritz
Max Planck Institute for Molecular Cell Biology and Genetics, Max Planck Society;

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Woodruff,  Jeffrey
Max Planck Institute for Molecular Cell Biology and Genetics, Max Planck Society;

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Citation

Mittasch, M., Tran, V. M., Rios, M. U., Fritsch, A., Enos, S., Gomes, B. F., et al. (2020). Regulated changes in material properties underlie centrosome disassembly during mitotic exit. The Journal of cell biology, 219(4): e201912036. doi:10.1083/jcb.201912036.


Cite as: https://hdl.handle.net/21.11116/0000-0008-A338-1
Abstract
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, before anaphase, PLK-1 and SPD-2 respectively 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.