Polo‐Like Kinase 1 Phosphorylation Tunes the Functional Viscoelastic Properties of the Centrosome Scaffold

Cytoskeleton‐organizing organelles often function while under mechanical load. The outer layer of centrosomes, called pericentriolar material (PCM), nucleates microtubules that move chromosomes during mitosis. How PCM resists microtubule‐mediated forces is poorly understood at the material level. This study shows that PLK‐1 phosphorylation of SPD‐5 tunes the dynamics and material properties of the PCM scaffold in C. elegans embryos. Microrheology of reconstituted SPD‐5 scaffolds reveals that PLK‐1 phosphorylation decreases SPD‐5 dynamics and increases scaffold viscoelasticity. Similarly, in embryos, phospho‐mimetic SPD‐5 is less dynamic than wild‐type SPD‐5, which itself is less dynamic than phospho‐null SPD‐5. PCM built with phospho‐null SPD‐5 is smaller than normal, but its assembly can be partially rescued by reducing microtubule‐dependent forces. The same is true for PCM built with phospho‐mimetic SPD‐5, yet the underlying causes are distinct: under force, phospho‐null SPD‐5 fails to assemble, while phospho‐mimetic SPD‐5 forms hyper‐stable foci that fail to cohere into a uniform, spherical mass. Both mutants have defects with chromosome segregation and viability. Thus, tuning of SPD‐5 phosphorylation optimizes PCM material properties to achieve correct PCM size, integrity, and function. These results demonstrate how regulated chemical modification of a scaffolding protein tunes the material properties and function of a microtubule‐organizing organelle.