McIdas localizes to centrioles and controls centriole numbers through PLK4-dependent phosphorylation.

The centriole duplication cycle must be tightly controlled and coordinated with the chromosome cycle. Aberrations in centriole biogenesis can cause developmental disorders, ciliopathies and cancer, yet the molecular determinants controlling centriole numbers and the link between the two cycles remain poorly characterized. Here, we demonstrate that McIdas, previously implicated in cell cycle regulation and multiciliogenesis, plays a critical role in maintaining proper centriole numbers. McIdas localizes to centrioles, where it exhibits dynamic localization throughout the cell cycle, dependent upon a nuclear export signal (NES) in its coiled-coil domain. Overexpression of McIdas induces centriole overduplication, whereas its depletion perturbs daughter centriole biogenesis and SAS6 recruitment. An NES mutant of McIdas that fails to localize to centrioles does not induce centriole amplification. Moreover, McIdas depletion reduces PLK4-induced centriole amplification. McIdas interacts with and is phosphorylated by PLK4, which is critical for its role in centriole number control. Overall, our results demonstrate that in addition to its known nuclear localization, McIdas also localizes to centrioles, affecting centriole duplication. This novel, direct role of McIdas in centriole duplication connects its functions in cell cycle regulation and multiciliogenesis.