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Ganuza et al. report that foetal liver haematopoietic stem cells (HSCs) are largely biased to differentiation rather than self-renewal, resulting in a modest expansion of the HSC pool with contribution to adult haematopoiesis.
Liu and Dekker test the importance of cohesin ring integrity for genome architecture: cohesin ring opening via Rad21 cleavage causes loss of CTCF–CTCF loops but maintains dynamic intra-domain loops, suggesting distinct cohesin engagement modes.
Banerjee et al. detail the spatial and temporal dynamics of the surface charge on the inner leaflet of the plasma membrane and show that these dynamics are necessary and sufficient to regulate signalling pathways mediating cell migration and polarity.
Larionova et al. identify a mechanism by which acidification of the tumour microenvironment within the glioblastoma core induces the generation of an alternative splice isoform of ribosomal protein RPL22L1, which regulates cell stemness and increases tumour heterogeneity.
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.
Bao et al. report that a cadherin code regulates the assembly and sorting of the first three cell lineages during mammalian development and can be manipulated to enhance the efficiency of synthetic embryogenesis.
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.
Zou et al. use a single multi-target guide RNA to direct Cas9 to a high number of loci mapped by high-throughput short-read sequencing. This multi-target CRISPR system allows detailed studies of genome editing and DNA repair.
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.