Jones et al. determine the role of matrix stiffness in regulating chromatin accessibility in freshly isolated lung fibroblasts. They identify ZNF416 as a key transcriptional regulator controlling fibroblast activation by the mechanical environment with relevance to wound healing and fibrosis.

Restricting the localization of CENP-A to centromeres is essential to prevent chromosomal instability (CIN). CENP-A is overexpressed and mislocalized in several cancers. Shrestha et al. show that overexpression of CENP-A leads to its mislocalization, CIN, and aneuploidy with karyotypic heterogeneity.

How protein endocytic recycling changes in response to environmental cues is poorly understood. Mao et al. demonstrated that multiple stresses inhibited endocytic recycling via MAPK11/14-mediated phosphorylation of SNX27 at Ser51. Phosphorylation of SNX27 decreases its binding to cargo proteins and suppresses protein endocytic recycling.

Junyent et al. describe how the cell communication through cytonemes that leads to synthetic embryogenesis is altered upon pluripotency state transition in stem cells. They show that in more developmentally advanced stem cells, Wnt-iGluR crosstalk in the cytonemes is impaired, resulting in reduced formation of synthetic embryo structures.

Balmer et al. identify a new player in the complex network of epigenetic modifiers safeguarding stem and progenitor cell pools in stratified epithelia. SUV39H2, an enzyme introducing repressive methyl marks on chromatin, governs the master switch of stem and progenitor cells during epithelial fate conversion.

Ubiquitin conjugation to histone lysines regulates diverse processes such as gene silencing, transcriptional elongation, and DNA repair. Combining an avidity-based design strategy with molecular dynamics simulations, dos Santos Passos et al. develop genetically encoded sensors for H2AK13/15 or H2BK120 ubiquitinated nucleosomes and use them in live cells to monitor ubiquitin-dependent signaling.

Structured illumination microscopy, cryo-ET, and computational analyses reveal that nuclear pore complexes (NPCs) and specific lamins spatially distribute in a codependent manner. Knocking out certain lamin genes or knocking down particular nucleoporins perturbs how both lamins and NPCs distribute in the nuclear envelope.