Quantitative experiments and theory show that the tension-dependent regulation of NDC80 binding to kinetochore microtubules arises from a combination of the changing Aurora B concentration at NDC80 and the nonlinearity of Aurora B autoactivation.

A biophysical model in which kinetochore microtubules nucleate at kinetochores and growth polward along nematic streamlines quantitatively explains kinetochore microtubule lengths, orientations, and spatially varying dynamics in metaphase human spindles.

The meiotic DNA recombination landscape is locally influenced by the kinetochore to minimize potentially deleterious pericentromeric crossover recombination.

STED microscopy of human mitotic spindles reveals how augmin-nucleated microtubules protect the cell from erroneous kinetochore-microtubule attachments and ensure a highly organized architecture of the spindle required for mitotic fidelity.

The outer domain of the kinetochore can rotate (swivel) around the centromere, and this rather than intra-kinetochore stretching is coupled to anaphase onset.

Distinct PP2A-B56 complexes use isoform-selective interactions to localise to either the centromere or kinetochore and control different processes during mitosis.

Preventing premature interactions between microtubules and protein-based structures called kinetochores ensures that chromosomes are segregated by meiosis rather than mitosis in reproductive cells.

Centromeric protein M (CENP-M) is required for the stabilization of a quaternary complex that plays a crucial role in kinetochore organization and function.

Multiple NDC80 complexes in the outer kinetochore cooperate to bind the ends of depolymerizing microtubules and harness their power stroke.

Multiple age-related changes in chromosome architecture could explain why human oocyte aneuploidy increases with advanced maternal age.