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Organ morphogenesis begins with proliferation, which results in tissue pressures and site-specific YAP expression, nuclear translocation and signalling. A study now reports the involvement of anisotropy, localized pressure and YAP signalling in organizer-forming cascades, introducing a new chapter of molecular mechanobiology of organogenesis.
Three studies identify a transcription-coupled DNA–protein cross-link repair pathway that depends on the Cockayne syndrome proteins and the proteasome.
Liu et al. find that long-chain acyl-coenzyme A activates two mitochondrial fission proteins, MiD49 and MiD51, by inducing their oligomerization. This activates their ability to stimulate DRP1 GTPase activity and triggers mitochondrial division.
Scarfò, Randolph et al. perform transcriptomic analysis of 28- to 32-day human embryos and identify CD32 as a marker of haemogenic endothelial cells (HECs), thus providing a strategy to isolate HECs from human embryos and pluripotent stem cell cultures.
Eukaryotic transcriptional machinery often shows local enrichment in dynamic clusters at sites of high expression. A study of zebrafish embryos shows that such clusters can fine-tune the timing of zygotic genome activation by sequestering a component required for productive transcription, thus limiting its availability to other genes.
Diverse, specialized immune cells defend against pathogens and cancer cells. A new study reveals the comprehensive lipid compositions of these cells, with unique lipidomes associated with various immune cell types. They show that cell-specific lipid compositions determine a key functional phenotype: their susceptibility to ferroptosis.
Morgan, Pernes and colleagues perform mass spectrometry-based targeted lipidomics and provide a comprehensive lipid profile of human and mouse immune cells, which they then show confer differential ferroptosis susceptibilities.
Ugolini et al. show that transcription bodies regulate gene expression during zygotic genome activation in zebrafish development by sequestering CDK9 to limit the transcription of genes away from transcription bodies.
Shroff and colleagues report that cell proliferation induces localized mechanical compression in the tissue, driving the formation of the main mouse tooth signalling centre via differential YAP expression.
Maneix, Iakova and colleagues report that cyclophilin A is a chaperone for, and regulator of, intrinsically disordered proteins within haematopoietic stem and progenitor cells, with potential effects on ageing-like phenotypes and lineage commitment.
Using single-molecule tracking and spatiotemporal mapping, Ling et al. show that the C-terminal domain of RNA polymerase II facilitates its dynamic confinement in subnuclear regions enriched in active genes, where it promotes targeted transcription.
Coquand, Brunet Avalos et al. develop an imaging method to map basal radial glial cell division in human fetal tissue and cerebral organoids and detect abundant symmetric amplifying, but also direct neurogenic divisions bypassing intermediate progenitors.
Progeria, or premature ageing, is a devastating condition caused by defects in the nuclear envelope and is associated with systemic inflammation. A study now shows in animal models that inhibiting necroptosis, and particularly activity of the RIPK1 kinase, reduces inflammation and results in a meaningful extension in lifespan1.
Despite the constant renewal of their components, cellular actin networks maintain their overall appearance, through a subtle balance of filament assembly and disassembly. This balance is key to the remodelling of cellular architecture. We discuss the significance of in vitro reconstitutions in deciphering the complexity of actin regulation.
Xu and colleagues identify a sequential palmitoylation–depalmitoylation mechanism that controls GSDMD cleavage by caspases, plasma membrane trafficking and oligomerization, thereby triggering pyroptosis in a spatial and temporal manner.
Yang, Zhang et al. identify a non-canonical form of necroptosis driven by nuclear RIPK1-mediated nuclear membrane rupture as a result of ZMPSTE24 deficiency and defective prelamin A processing commonly observed in progeroid disorders.