The lamin A/C binding protein LAP2α inhibits formation of higher order lamin structures in the nuclear interior in a lamin A/C-phosphorylation-independent manner, thereby regulating chromatin mobility.
The histone modification H3K9me2 marks peripheral heterochromatin and ensures positional information is safeguarded through cell division such that individual lamina-associated domains are re-established at the nuclear periphery in daughter nuclei.
The INM protein LAP1B, an activator of Torsin ATPases, is a chromatin-binding factor that erroneously persists on mitotic chromatin if Torsin functionality is compromised, inducing chromosome segregation defects and binucleation.
Combined light and electron microscopy reveals a new function for Arp2/3-mediated actin assembly in nuclear envelope rupture, which leads to a separation of nuclear membranes and pores from the lamina.
Knockout of the methyltransferase ICMT prevents progerin methylation and improves survival in mice with Hutchinson-Gilford progeria syndrome (HGPS) and an ICMT inhibitor delays senescence and stimulates proliferation of HGPS cells.
Models that generate tandem alignments of cell polarities are more readily compatible with the formation of PIN1 polarity patterns in plant leaf buds than the most widely accepted “up-the-gradient” model.