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

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.

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.

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.

Human chromosome-microtubule attachments are stabilised by Astrin-mediated dynamic delivery of PP1 phosphatase to the attachment site, which ensures the normal segregation of chromosomes.

The structural maintenance of chromosomes complex, SMC5/6, is crucial for brain development and function as it ensures proficient DNA replication in neural progenitor cells prior to chromosome segregation.

The INM protein LAP1B, an activator of Torsin ATPases, is a chromatin-binding factor that erroneously persists on mitotic chromatin if Torsin functionality is compromised, inducing chromosome segregation defects and binucleation.

A structural and biochemical approach shows that CTP binding and hydrolysis regulate nucleation, spreading, and recycling of a chromosome segregation protein ParB.

Cell biological and genetic analyses reveal how budding yeast cells optimize Spindle Assembly checkpoint signaling to maximize chromosome segregation accuracy and minimize unnecessary delays in anaphase onset.