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Wesley et al. describe the developmental trajectories of human foetal liver cell types at single-cell resolution and generate bipotential hepatoblast organoids, which can serve as a new platform to investigate human liver development.
Lanna and colleagues discover extracellular vesicle-mediated transfer of telomeres from antigen-presenting cells to T cells, which enables elongation of chromosomes, protection against replicative senescence and long-term immune defence.
Gollwitzer, Grützmacher et al. and Figlia et al. establish that the various Rag GTPase genes and isoforms differentially regulate mTORC1 activity and distinctly modulate the responsiveness of mammalian cells to amino acid availability.
Gollwitzer et al. and Figlia et al. establish that the different Rag GTPase genes and isoforms differentially regulate mTORC1 activity and distinctly modulate the responsiveness of mammalian cells to amino acid availability.
Lu et al. report that biomolecular condensation of cytoplasmic TDP-43 is regulated by HSPB1 to maintain its droplets in liquid and not gel/solid structures and that HSPB1 is decreased in spinal motor neurons with TDP-43 pathology in patients with amyotrophic lateral sclerosis.
Huyghe, Furlan et al. compare pluripotent reprogramming with oncogenic transformation and identify Bcl11b and Atoh8 as regulators of cellular plasticity in both processes, thus offering a unifying theory on the factors constraining cell fate changes.
Song et al. identify two protein-targeting pathways from the endoplasmic reticulum to (1) early lipid droplets (LDs) and (2) mature lipid droplets. They define key factors mediating the second, late pathway and its many cargoes.
Nguyen et al. show that the E3 ubiquitin ligase MARCHF6 acts as an NADPH sensor to suppress ferroptosis. Mechanistically, NADPH binds to MARCHF6 and activates its E3 ligase activity, enhancing the degradation of pro-ferroptosis proteins.
Sahu et al. show that ZNF827 is essential for epithelial-to-mesenchymal transition in breast cancer metastasis and cortical development. Mechanistically, ZNF827 controls RNA splicing landscape by recruiting HDAC1 to slow RNA polymerase II progression.
Diehl et al. show that imbalance among nucleotide species is not sensed by canonical metabolic regulatory pathways, causing excessive cell growth despite a DNA replication block. ATR is needed to increase nucleotide availability in normal S phase.
Wei et al. identify that cytoplasmic METTL3 interacts with PABPC1 to facilitate translation of epigenetic factor mRNAs without m6A modification to promote tumour progression, suggesting an m6A-independent mechanism for this methyltransferase.
Guo et al. show that ligand-induced EGFR activation suppresses invasion by upregulating BIN3 and inhibiting DOCK7-regulated Rho GTPase activity in EGFR-amplified glioblastoma, which is in contrast to the known oncogenic role for EGFR signalling.
Chandrakanthan et al. identify Mesp1-derived PDGFRA+ stromal cells as aortic endothelial precursors that regulate long-term haematopoietic-stem-cell generation during development, thus providing a new potential tool to generate engraftable haematopoietic stem cells.
Lin, Swedlund et al. report that Mesp1 governs the remodelling of the chromatin and enhancer landscape during differentiation of early mesodermal cells into distinct populations of cardiovascular progenitors.
Emam et al. report that Abro1 and FANCD2 protect stalled replication forks from degradation, thereby preventing the accumulation of cytosolic ribosomal DNA and the activation of cGAS–STING- and P-body-dependent innate immune responses.
Mylvaganam et al. report that an apical spectrin network in endothelial cells can transmit mechanical forces in response to shear flow-induced stress, requiring hyaluronic acid and involving PIEZO1.
Chen et al. report that following genotoxic stress, a nuclear PI3K binds p53 to generate a p53–phosphoinositide signalosome that recruits AKT and its activators, resulting in nuclear AKT activation and cell survival.
Yang et al. report that HHEX acts as a gatekeeper of pancreatic lineage specification against the liver and duodenum fates via guiding FOXA1, FOXA2 and GATA4 to activate pancreatic genes, while restraining them from activating alternative lineages.