Identifying Centriole-associated Factors That Induce Differentiation

The centrosome is fundamentally recognized for its role in cell division and ciliogenesis. However, emerging evidence suggests a non-canonical function: the centriole, particularly the mother centriole, acts as a regulatory hub for cellular differentiation. This article synthesizes data from 65 studies (2010–2024) to test the hypothesis that centrioles are associated with unique sets of regulatory molecules which, upon specific cues, can act as local inducers of cell fate. We systematically identify and classify such Centriole-Associated Fate Determinants (CAFDs), including transcription factors (STAT3, YAP/TAZ, Gli), RNA regulators (Prospero mRNA), kinases (PLK4), and ubiquitin ligase components. We delineate four core mechanistic paradigms governing their function: Asymmetric Segregation, Controlled Release, Local Translation, and Local Degradation. A comparative analysis across neurogenesis, gliogenesis, myogenesis, and mesenchymal differentiation reveals both conserved principles and lineage-specific adaptations of these mechanisms. We further review critical methodological approaches—from centrosomal proteomics to proximity ligation (BioID/APEX) and mRNA-trapping—essential for discovering CAFDs. Finally, we propose an integrative "Centriolar Decision-Making Conveyor" model, positioning this organelle as an active processing station that integrates signals and dispatches instructive cues to the nucleus. This refines our understanding of cell fate specification and highlights the therapeutic potential of manipulating centriolar signaling to direct differentiation in regenerative medicine and oncology.