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.
Highlights
Centrosomes nucleate and anchor microtubules that make up possibility is that an increase in cortical forces during mitotic exit the mitotic spindle, which segregates chromosomes during so- induces centrosome disassembly
focused light-induced cytoplasmic streaming (FLUCS) reveals weakening of the pulling forces also occurs in metaphasematerial (PCM) scaffold at anaphase onset in C. elegans embryos To study the molecular determinants of PCM load-bearing capacity, we studied C. elegans one-cell embryos, in which growth and disassembly of the PCM scaffold are visualized using fluorescently labeled SPD-5
Our results reveal that PCM composition changes in a stepwise manner during anaphase: PLK-1 departs first, followed by SPD-2, γ-tubulin, transforming acid coiled coil protein 1 (TAC-1), and SPD-5 and proteins that form tight complexes with SPD-5
Summary
Centrosomes nucleate and anchor microtubules that make up possibility is that an increase in cortical forces during mitotic exit the mitotic spindle, which segregates chromosomes during so- induces centrosome disassembly. PCM carries out most of the functions of a arrested embryos without leading to centrosome deformation centrosome, including directing cell polarity, cell migration, and or fracture (Labbeet al., 2004). These studies suggest that induction of centrosome microtubule-dependent loads that create tensile stresses. Motor deformation and fracture during mitotic exit cannot be suffiproteins anchored at the plasma membrane attach to and walk ciently explained by increased microtubule-mediated forces
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