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The discovery of non-canonical telomeric dsDNA-binding proteins in Caenorhabditis elegans reveal their contribution in the maintenance of telomere length and germline immortality.

In vitro, in vivo and in silico evidence suggests that bacteria exploit intrinsic chromosomal fluctuations to achieve intracellular transport.

The kinetoplastid parasite Trypanosoma brucei employs a unique mechanism to target the conserved Aurora B kinase to kinetochores and the central spindle.

Internally tagged, functional Cse4/CENP-A/CenH3 histone variant is exclusively centromeric and stable through the budding yeast cell cycle after replacement in S phase.

A chromosome-wide mechanism balances X-linked gene expression between the sexes in C. elegans, but no similar chromosome-wide mechanism balances gene expression between X chromosomes and autosomes.

A sharp transition in the fate of DNA ends with telomere sequences is identified, which suggests a boundary between DNA double-strand breaks and telomeres.

AurkA is imported into mitochondria at interphase, and it induces organelle elongation and enhances ATP production when over-expressed.

Building on previous work (Tang et al., 2015), novel ESCRT-III subunit Snf7 auto-activation mutants are used to reveal two parallel ubiquitin-dependent pathways during multivesicular endosome biogenesis.

A method to generate human cells with massive chromosomal aberrations on a specific chromosome allows analysis of their consequences.

Large regions of foreign DNA inserted into mammalian chromosomes assemble into H3K9me3-heterochromatin and result in increased condensin loading with organisation into shorter mitotic chromosome loops than endogenous DNA.