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Dondelinger et al. and Menon et al. show that MAPKAP kinase-2 (MK2) phosphorylates RIPK1 to regulate TNF-mediated cell death as well as RIPK1 signalling in inflammation and bacterial infection.
Lee et al. found that the ubiquitin-editing enzyme A20 promotes TGF-β1-induced EMT and metastases of breast cancer cells via ubiquitylation-mediated nuclear stabilization of Snail1.
Zhuang et al. show that breast-cancer-secreted DKK1, while promoting bone metastases via canonical WNT signalling, inhibits lung metastasis by antagonizing non-canonical Wnt signalling to suppress recruitment of anti-tumour immune cells.
McNally et al. identify the retriever complex as required for endosomal cargo recycling. Retriever binds SNX17, the CCC and WASH complexes to govern cell surface expression of integrins, receptors and transporters.
Roman et al. demonstrate that crosslinking and contraction of myofibrils mediate the movement of nuclei to the periphery of myofibres, and describe a role for Arp2/3 in organizing desmin.
Saad et al. identify stress-induced reversible protein aggregation as a protective mechanism to ensure cell cycle resumption and cell survival after stress in yeast.
Shi et al. map the ciliary transition zone by STORM imaging, characterizing protein arrangements in nested rings and finding that mutations in RPGRIP1L that are associated with the ciliopathy Joubert syndrome disrupt SMO ciliary localization.
Tait and colleagues show that caspase-independent cell death induced by mitochondrial permeabilization stimulates NF-κB activity through downregulation of inhibitor of apoptosis, and enhances anti-tumour effects.
Skamagki et al. show that pluripotency factor ZSCAN10 is poorly expressed in iPSCs derived from aged donors, and its addition during reprogramming restores the DNA damage response and genomic stability through normalization of ROS–glutathione levels.
Grelet et al. find that hnRNP E1 release from PNUTS pre-RNA in response to TGFβ generates a lncRNA that acts as competitive sponge for miR-205, promoting epithelial–mesenchymal transition in cancer.
Horton et al. show that early Crebbp loss in haematopoietic progenitors results in a defective p53-mediated DNA damage response, leading to the accumulation of epigenetic and genetic alterations, which promote the onset of lymphoid malignancies.
Zihni et al. discover a role for Cdc42–MRCK signalling in establishing contractility at the apical pole, which in turn controls epithelial polarity in mammalian cells and Drosophila photoreceptors.
Schalbetter et al. show by Hi-C and modelling that mitotic chromosome compaction in budding yeast occurs by cis-looping of chromatin, and reveal distinct roles for cohesin and condensin depending on chromatin context.
Flores et al. show that hair follicle stem cells rely on the production of lactate via the LDHA enzyme to become activated. Inducing Ldha through Mpc1 inhibition or Myc activation successfully reactivates the hair cycle in quiescent follicles.
Schell et al. demonstrate that inactivation of the mitochondrial pyruvate carrier in mouse and fly intestinal stem cells (ISCs) locks the cell into a glycolytic metabolic program and promotes the expansion of the stem cell compartment.
Hiraike et al. identify nuclear factor I-A (NFIA) as a transcriptional regulator of brown fat. NFIA activates cell-type-specific enhancers prior to differentiation and facilitates PPARγ binding to regulate the brown fat gene program.
Glück et al. find that the DNA-sensing component cyclic GMP-AMP synthase (cGAS) recognizes cytosolic chromatin fragments produced in senescent cells leading to STING-mediated production of SASPs, which promotes paracrine senescence.
Xi et al. show that after influenza infection, hypoxia drives Notch signalling to expand Krt5+ basal-like cells in the lung. On HIF1α loss, epithelial progenitors directly differentiate into alveolar type II cells and promote functional regeneration.
Joyce and colleagues report that obesity promotes lung neutrophilia in mice, which in the presence of a primary breast tumour fosters metastasis to the lung in a manner dependent on GM-CSF and IL5.
Bitler et al. show that HDAC6 activity is essential for the survival of ovarian cancer cells carrying loss-of-function ARID1A mutation, thus representing a promising therapeutic target.