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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.
Duan et al. show that ACE2-dependent and ACE2-independent entry of SARS-COV-2 in epithelial cells versus myeloid cells differentially regulates viral replication and inflammatory responses, thereby contributing to COVID-19 progression and pathology.
β-propeller protein-associated neurodegeneration (BPAN) is caused by loss of functional WIPI4. A new study reports that depletion of WIPI4 induces ferroptosis via changes in mitochondrial membrane lipids, independently of the role of WIPI4 in autophagy, providing insights into the cause of neurodegeneration in BPAN.
Zhu et al. show that loss of WIPI4, as seen in β-propeller protein-associated neurodegeneration, causes ferroptosis independently of autophagy due to an imbalance in phosphatidylethanolamine levels.
Mathiowetz and Olzmann review our current understanding of the mechanisms of lipid droplet biogenesis and turnover, the transfer of lipids and metabolites at membrane contact sites, and the role of lipid droplets in regulating fatty acid flux in lipotoxicity and cell death.