Lis1-dynein drives corona compaction and limits erroneous microtubule attachment at kinetochores.

Mitotic cell division requires that kinetochores form microtubule attachments that can segregate chromosomes and control mitotic progression via the spindle assembly checkpoint. During prometaphase, kinetochores shed a domain called the fibrous corona as microtubule attachments form. This shedding is mediated, in part, by the minus-end directed motor dynein, which 'strips' cargoes along K-fibre microtubules.

CENP-F stabilizes kinetochore-microtubule attachments and limits dynein stripping of corona cargoes.

Accurate chromosome segregation demands efficient capture of microtubules by kinetochores and their conversion to stable bioriented attachments that can congress and then segregate chromosomes. An early event is the shedding of the outermost fibrous corona layer of the kinetochore following microtubule attachment. Centromere protein F (CENP-F) is part of the corona, contains two microtubule-binding domains, and physically associates with dynein motor regulators.

Congressing kinetochores progressively load Ska complexes to prevent force-dependent detachment.

Kinetochores mediate chromosome congression by either sliding along the lattice of spindle microtubules or forming end-on attachments to their depolymerizing plus-ends. By following the fates of individual kinetochores as they congress in live cells, we reveal that the Ska complex is required for a distinct substep of the depolymerization-coupled pulling mechanism. Ska depletion increases the frequency of naturally occurring, force-dependent P kinetochore detachment events, while being dispensable for the initial biorientation and movement of chromosomes.

Building an integrated model of chromosome congression.

A universal feature of mitosis is that all chromosomes become aligned at the spindle equator--the halfway point between the two spindle poles--prior to anaphase onset. This migratory event is called congression, and is powered by centromere-bound protein machines called kinetochores. This Commentary aims to document recent advances concerning the two kinetochore-based force-generating mechanisms that drive mitotic chromosome congression in vertebrate cells: depolymerisation-coupled pulling (DCP) and lateral sliding.

Chromosome congression is promoted by CENP-Q- and CENP-E-dependent pathways.

A key step of mitosis is the congression of chromosomes to the spindle equator. Congression is driven by at least two distinct mechanisms: (1) kinetochores slide along the microtubule lattice using the plus-end directed CENP-E motor, and (2) kinetochores biorientating near the pole move to the equator through microtubule depolymerisation-coupled pulling. Here, we show that CENP-Q - a subunit of the CENP-O complex (comprising CENP-O, CENP-P, CENP-Q and CENP-U) that targets polo-like kinase (Plk1) to kinetochores - is also required for the recruitment of CENP-E to kinetochores.