Centrosome articles from across Nature Portfolio

Centrioles are characterized by an atypical triplet microtubule structure. Here, the authors discover that the ciliopathy protein HYLS1 promotes the assembly of triplet microtubules within human centrioles.

Centrioles have a conserved structure and function but have diversified in sperm. Here the authors provide insight into the molecular mechanisms and adaptive evolution underlying this diversification.

The dynein motor complex has a variety of important functions in both dividing and non-dividing cells. Here, Gallisà et al. describe a mode of regulation of dynein based on the phosphorylation of its adaptor BICD2 by the kinase PLK1, and how this is central for the regulation of centrosome position in G2 and M.

The authors find that the ciliopathy-associated protein Oral-Facial-Digital syndrome 1 functions as a class II nucleation promoting factor to drive actin filament branching, required for cell cycle progression. Interferring with this function suppresses cancer cell growth.

The molecular mechanisms underpinning the organization of microtubule arrays remain unclear. Here the authors show that in human cells, the microtubule polymerase ch-TOG promotes nucleation of microtubules at the interphase centrosome and the Golgi through a mechanism that involves transient interaction with the microtubule nucleator γTuRC.

ESCRT-III seals holes in the nuclear envelope (NE). A study now shows that the Cmp7-directed ESCRT-III cascade that grommets and reseals NE holes after spindle pole body (SPB) extrusion at the end of fission yeast mitosis is complemented by the presence of a proteinaceous diffusion barrier to ensure NE integrity.

Overload of proteasomal clearance triggers formation of a large protein inclusion called the aggresome, which shares similarities with protein aggregates seen in neurodegenerative diseases such as Huntington’s. A new study uncovers how centrosome and centriolar satellite components facilitate stepwise assembly of aggresomes.

Assembly of the mitotic spindle requires timely separation of the centrosomes. Their movement apart is driven by the plus-end-directed kinesin Eg5. A new study demonstrates that the kinesin KIFC3 provides an opposing microtubule-based cohesive force that modulates centrosome separation and ensures accurate chromosome segregation.

Two papers demonstrate that centrosome amplification can cause cancer in mammals and that a PIDDosome–p53-dependent control mechanism acts to prevent cell proliferation in the presence of extra centrosomes.

Three independent studies provide molecular insights into the mechanism governing cell cycle arrest in response to centrosome loss.

Centrosomes can nucleate not only microtubules but also actin filaments, in a process dependent on the actin-related protein 2/3 complex and WASH.