Centromeres articles from across Nature Portfolio

FBXO47 is key component of the centromeric SCF E3 ligase complex that regulates centromere pairing for pachynema progression in mouse spermatocytes.

Helsen et al. use experimental evolution and chromosome engineering to probe the link between karyotype changes and the cell division machinery. They conclude that spindle organization dictates the available trajectories for karyotype evolution.

This publication provides the first quantitative description of rapid chromosome movements during A. thaliana meiotic prophase. It also shows that they depend on the SUN1 and SUN2 proteins and correlate with major nuclear envelope rearrangements.

How RNA polymerase II transcription of tandemly repetitive satellite DNAs is regulated is poorly understood. Here, the authors identify Topoisomerase I as an evolutionary key regulator for satellite DNA transcription under both normal and DNA double-stranded break conditions.

A comparison of two complete sets of human centromeres reveals that the centromeres show at least a 4.1-fold increase in single-nucleotide variation compared with their unique flanks, and up to 3-fold variation in size, resulting from an accelerated mutation rate.

Logsdon et al. report the second complete sequence of all centromeres from a single human genome, enabling comparative analyses of the variation in tandemly repeating α-satellite DNA.

Centromere identity must be maintained through multiple generations. A new study reveals a Constitutive Centromere-Associated Network (CCAN)-dependent retention of CENP-A, a key epigenetic mark for centromeres, in centromeres during DNA replication and a replication-dependent error correction to eliminate ectopic CENP-A in chromosome arms.

Tubulin in meiotic oocyte spindles is asymmetrically tyrosinated, and this spindle asymmetry can drive biased, non-Mendelian inheritance of chromosomes.

Micronucleation of missegregated chromatin can lead to substantial chromosome rearrangements via chromothripsis. However, the molecular details of micronucleus-based chromothripsis are still unclear. Now, an elegant system that specifically induces missegregation of the Y chromosome provides insight into this process, including a role for non-homologous end joining.