PCM1 intrinsically forms multimerized granules and acts as the core organizing scaffold, with its activity regulated by the cytoskeleton and ciliary-disease–associated proteins.

PCM1 alone is sufficient to form an internal scaffold, selectively recruit specific proteins, and interact with microtubules, linking centriolar satellites to the cellular transport system.

Researchers developed new cellular and in vitro systems to observe centriolar satellite biogenesis, revealing distinct assembly, remodeling, and maintenance stages.

The work was funded by the European Research Council, TÜBİTAK, and the Istanbul Development Agency.

The study introduces experimental tools to study membrane-less organelles step by step, offering a framework to investigate other organelles and disease-related disruptions in cellular architecture.

Koç University-led research shows centriolar satellites assemble through a highly ordered, hierarchical process with PCM1 at the central scaffold.

Centriolar satellites contribute to cilia formation and function, with defects in PCM1 or other satellite proteins linked to vision loss, kidney disease, developmental disorders, schizophrenia, and microcephaly.

Disrupting PCM1 assembly impairs proper satellite formation and affects key cellular signaling pathways and cell division, underscoring the importance of hierarchical biogenesis.

High-resolution imaging reveals a nonuniform internal architecture of centriolar satellites, with PCM1 and recruited proteins occupying distinct subdomains as active organizational hubs.

PCM1 first forms a scaffold that sequentially recruits other satellite proteins, establishing defined stages of assembly, remodeling, and maintenance.