Modeling protein dynamics in Caenorhabditis elegans embryos reveals that the PLK-1 gradient relies on weakly coupled reaction–diffusion mechanisms

Protein gradients have fundamental roles in cell and developmental biology. In the one-cell Caenorhabditis elegans embryo, the mitotic Polo-Like Kinase 1 (PLK-1) forms an anterior-rich cytoplasmic gradient, which is crucial for asymmetric cell division and embryonic development. The PLK-1 gradient depends on the RNA-binding Muscle-EXcess-5 protein (MEX-5), whose slow-diffusing complexes accumulate in the anterior via a reaction–diffusion mechanism. Here, we combine experiments and a computational approach to investigate the dynamics of PLK-1 gradient formation. We find that the gradient of PLK-1 initiates later, is less steep, and forms with slower dynamics than does the MEX-5 gradient. The data show that PLK-1 diffuses faster than MEX-5 in both anterior and posterior cytoplasmic regions. Our simulations suggest that binding to slow-diffusing MEX-5 is required for PLK-1 gradient formation, but that a significant fraction of unbound PLK-1 is necessary to justify the different gradient dynamics. We provide a computational tool able to predict gradient establishment prior to cell division and show that a two-component, bound and unbound, model of PLK-1 dynamics recapitulates the experimental observations.