Mitosis articles from across Nature Portfolio

Lipid synthesis increases during the cell cycle to ensure sufficient membrane mass. Here, authors identify a lipid checkpoint in G1 phase that prevents cells from starting the cell cycle if lipid synthesis is low, thereby preventing mitotic defects.

The Eyes Absent proteins (EYA1-4) are a group of tyrosine phosphatases. Here, the authors report a signalling pathway in which EYA4 and EYA1 dephosphorylate Polo-like kinase 1 (PLK1) at pY445 to support PLK1 activation and mitosis.

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.

The collapse of DNA replication forks leads to the formation of single-ended DNA double-strand breaks. One would have assumed that these breaks would be repaired as soon as possible. However, a recent study suggests that a delay in DNA polymerase θ-mediated end joining until mitosis, orchestrated by BRCA2 and RAD52, favors genomic stability.