Aneuploidy can cause chromosome mis-segregation and specific cellular phenotypes driven by expression of genes on the extra chromosome.

The presence of cenexin at the old centrosome imposes a functional asymmetry on the mitotic spindle that impacts chromosome alignment and segregation.

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

Contrary to the generally accepted model, condensin maintains proper gene expression by promoting the accurate segregation of chromosomes and the partitioning of the RNA-exosome throughout mitosis, instead of directly regulating transcription.

Chemical inhibition of Bub1 shows that the catalytic activity is not required for normal mitotic progression, but it makes chromosome segregation and cell proliferation more sensitive to the effects of the anti-cancer drug Paclitaxel.

A combination of structural, biochemical, single-molecule and in vivo methods are used to show how ParB locally condenses the bacterial chromosome near the origin and earmarks this region for segregation.

During chromosome segregation, BUB-1 performs multiple roles.

Condensation and segregation of chromosomes during mitosis is caused by a combination of short-range interactions between nucleosomes and the long-range contraction of chromosome arms mediated by condensin.

The chromosomal passenger complex interacts with the inner kinetochore COMA complex through the Ctf19 C-terminus in vitro which is shown to be important for mediating accurate chromosome segregation.

Extensive cytological and biochemical analyses show that the conserved Sf3A2 and Prp31 splicing factors bind microtubules and the Ndc80 complex, playing direct mitotic functions in both Drosophila and human mitosis.