Mitosis articles from across Nature Portfolio

The nuclear localization of metabolic enzymes is fascinating and in most cases remains a mystery. Here, Pardo Lorente and colleagues show that nuclear MTHFD2 is required for successful mitosis by controlling centromeric histone methylation.

Metaphase chromosomes oscillate while attached to growing and shrinking microtubules. Here, the authors show that an α-tubulin detyrosination gradient on kinetochore microtubules fine-tunes load-bearing attachments during chromosome oscillations.

Novel layer of regulation on BubR1-Plk1 interaction via Plk1 self-priming ensures proper mitotic progression.

The mechanisms of nonrecurrent structural variant (SV) formation are poorly understood. Here, the authors sequenced thousands of SV junctions as they formed at common fragile sites in human cell lines to reveal a primary role for DNA polymerase theta-mediated end joining activated during mitosis.

Transcriptome-wide profiling studies in mammalian cells show that the stringency of start-codon selection is increased during mitosis, and that this is regulated by nuclear eIF1 to preserve mitotic arrest physiology.

In this Tools of the Trade article, Cao (Baskin lab) discusses the development of MARS, which enables mitosis-specific recruitment of enzymes to the plasma membrane, exploiting the cell cycle’s natural regulation of PLEKHA5 phosphorylation.

Ahna Skop and Karen Schindler describe a paper that found localized translation in mammalian embryos, demonstrating the importance of RNA transport for development.

Rapid reactivation of gene expression following mitosis-induced silencing is facilitated by a network of redundantly acting nuclear receptors that function as mitotic bookmarks.

DNA polymerase θ (POLQ) repairs mitotic DNA breaks; this requires RHINO and PLK1, averts genomic instability and may underlie effects of POLQ inhibitors in HDR-deficient cancer cells. We discuss recent work on mitotic DNA break processing and repair, the need for multiple DSB repair pathways and implications of therapeutic POLQ targeting in cancer.

ESCRT-III seals holes in the nuclear envelope (NE). A study now shows that the Cmp7-directed ESCRT-III cascade that grommets and reseals NE holes after spindle pole body (SPB) extrusion at the end of fission yeast mitosis is complemented by the presence of a proteinaceous diffusion barrier to ensure NE integrity.

Subunits of the SWI/SNF chromatin remodelling complexes ‘bookmark’ cell-type specifying genes during mitosis to allow their timely reactivation upon mitosis exit.