PLK1 controls centriole distal appendage formation and centrobin removal via independent pathways

Abstract

AbstractCentrioles are central structural elements of centrosomes and cilia. They originate as daughter centrioles from existing centrioles in S-phase and reach their full functionality with the formation of distal and subdistal appendages two mitoses later. Current models postulate that the centriolar protein centrobin acts as placeholder for distal appendage proteins that must be removed to complete distal appendage formation. Here, we investigated in non-transformed human epithelial cells the mechanisms controlling centrobin removal and its effect on distal appendage formation. We demonstrate that centrobin is removed from older centrioles due to a higher affinity for the newly born daughter centrioles, under the control of the centrosomal kinase Plk1. Centrobin removal also depends on the presence of subdistal appendage proteins on the oldest centriole. It is, however, not required for distal appendage formation even though this process is equally dependent on Plk1. We conclude that during centriole maturation, Plk1 kinase regulates centrobin removal and distal appendage formation via separate pathways.