Chromosome segregation articles from across Nature Portfolio

Using cryo-electron tomography, Dendooven et al. determined the structure of the native budding yeast γ-tubulin ring complex (γTuRC) capping spindle microtubules and showed that γTuRC adopts an active closed conformation to function as a perfect geometric template for microtubule nucleation.

Here, the authors determine the structure of the human outer kinetochore KMN network complex, showing that it forms an extended and rigid rod-like structure and that it exists in an auto-inhibited state which can be relieved by phosphorylation.

Mitotic spindle assembles in each blastomere to segregate duplicated chromosomes during cleavage of the fertilized egg. Here, the authors establish functional assays in fish embryos and find that Ran-GTP assembles a microtubule network at the metaphase spindle center that is essential for chromosome segregation.

Sissoko et al. show that CENP-T local concentration regulates its ability to recruit the outer kinetochore, which may restrict complete kinetochore formation to regions with higher-order inner kinetochore assemblies.

This study reveals that oxidative aneuploid cancer cells exhibit an upsurge of NADPH levels during mitosis, which neutralizes excessive reactive oxygen species and protects against chromosome mis-segregation.

A genome-wide CRISPR screen finds CIP2A as a new synthetic lethal target for BRCA1- and BRCA2-deficient cells. Unlike PARP inhibition that increases replication-induced DNA double-strand breaks and radial chromosomes, depleting CIP2A or disrupting its interaction with TOPBP1 increases micronuclei and chromosomal missegregation, revealing a mitotic target for BRCA-mutated tumors.

Suppressing ovulation protects against chromosomal abnormalities in ageing mouse oocytes, which can be partly explained by increasing REC8–cohesin retention on chromosomes.

Chromosomal instability (CIN) is a hallmark of malignant evolution that underpins cancer progression and therapeutic evasion. There are few established experimental systems to study CIN and ultimately develop potential therapeutic options. A new study now identifies the MSL chromatin complex as a potential vulnerability against CIN in cancer cells.

Liver cancer typically arises after years of inflammatory insults to hepatocytes. These cells can change their ploidy state during health and disease. Whilst polyploidy may offer some protection, new research shows it may also promote the formation of liver tumours.