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Esposito et al. report a role for bone vascular niche E-selectin in promoting mesenchymal–epithelial transition and Wnt signalling in breast cancer cells, thereby enhancing bone metastasis.
Unlike many other formin actin assembly factors, INF2 is not autoinhibited. Higgs and colleagues find that INF2 is inhibited by cyclase-associated protein and acetylated actin through a mechanism they name facilitated autoinhibition.
Chu et al. identify the lipoxygenase ALOX12 as essential for p53-dependent ferroptosis in a pathway independent of GPX4. Monoallelic deletion of Alox12 abrogates p53-mediated suppression in a model of Eµ-Myc-driven lymphoma.
Romeo et al. demonstrate that endochondral bone formation relies on proteolytic functions of type H endothelial cells, which interact with and support non-bone-resorbing, vessel-associated osteoclasts, a previously unrecognized cell type.
Chen et al. show that tumour-associated macrophages transmit HIF-1α-stabilizing long noncoding RNA through extracellular vesicles to breast cancer cells, thereby enhancing tumour glycolysis and chemoresistance.
Nguyen et al. show that neuropsin (OPN5) suppresses hyaloid vessel regression in the developing mouse retina in response to light, by regulation of the dopamine reuptake transporter and DRD2-dependent suppression of VEGFR2 activity.
Sengupta et al. show that protein sorting into the membranes of budding HIV particles is dependent on lipid-based partitioning of proteins, through a mechanism initiated by HIV protein Gag oligomerization at viral assembly sites.
Boos et al. show that impairing mitochondrial protein import induces a global transcriptional response to activate the ubiquitin–proteasome system and heat stress response and repress oxidative phosphorylation genes.
Choi et al. show that the stability of nuclear stress-activated wild-type and mutant p53 is regulated by the type I phosphatidylinositol phosphate kinase PIPK1-α and the lipid messenger PtdIns(4,5)P2.
Salvagno et al. demonstrated that blocking tumour-associated macrophages in breast cancer enhances the efficacy of chemotherapeutics by promoting intratumoural type I interferon responses.
Zhao et al. find that AMPK phosphorylates and activates the mitochondrial Ca2+ uniporter in response to low energy status in mitosis, allowing Ca2+ entry into mitochondria to boost mitochondrial respiration.
Jung et al. demonstrate, using 3D organoid cultures, that the PAR–aPKC polarity complex counteracts epithelial–mesenchymal transition and invasion through phosphorylation-dependent regulation of SNAI1 stability.
Nakamura et al. show that DNA repair pathway choice and initiation of homologous recombination is guided by the recruitment of BRCA1 to post-replicative chromatin by BARD1 recognition of histone H4 tails unmethylated on lysine 20.
Şentürk et al. show that ubiquilins bind v-ATPase to control lysosome acidity, mTOR signalling and autophagic flux in neurons, and that feeding flies with acidic nanoparticles ameliorates defective autophagy in ubiquilin mutants.
Wang et al. developed an inducible CRISPR–Cas9 system, in which guide RNA release is controlled by specific microRNAs, and demonstrated its application as a microRNA sensor and cell-type-specific genome regulator.
Spies et al. report that 53BP1 nuclear bodies restrain duplication of under-replicated DNA until the late S phase, thus promoting RAD52-mediated repair of these lesions.
Nacarelli et al. show that the nicotinamide-phosphoribosyltransferase-regulated NAD+ biogenesis pathway promotes the proinflammatory senescence-associated secretory phenotype by enhancing glycolysis and mitochondrial respiration during senescence.
Liu et al. show that the adaptive branch of unfolded protein response signalling, IRE1α–XBP1, protects haematopoietic stem cells and N-Ras pre-leukaemic stem cells from endoplasmic reticulum stress-induced apoptosis and supports their self-renewal.
Lystad et al. identify distinct membrane binding regions in ATG16L1 and show that the β-isoform-specific C-terminal region is required for VPS34/ULK1/2-independent non-canonical autophagy.