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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.
Lin et al. find that stress-induced p38 MAPK activation leads to cytoplasmic relocation of the Hippo pathway nuclear transcription factor TEAD. TEAD relocation causes inhibition of YAP activity and suppresses YAP-driven cancer cell growth.
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.
Studying polarity establishment in C. elegans zygotes, Wang et al. find, by imaging GFP-tagged proteins, that clusters of the PAR-3 polarity protein assemble in response to membrane tension created by actomyosin contractility.
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.
Hanssen et al. show that CTCF–cohesin binding sites at the α-globin gene cluster function as boundaries to restrict the interaction of enhancers with the flanking chromatin, thus preventing abnormal gene expression.
Zhou et al. demonstrate that bone marrow adipocytes, but not intraperitoneal adipocytes, express high levels of stem cell factor (SCF), which is essential for the regeneration of haematopoietic stem cells and haematopoiesis after irradiation.
Pitulescu et al. and Hasan et al. show that Dll4–Notch signalling in endothelial tip cells regulates angiogenesis through control of artery formation, linking sprouting angiogenesis and artery formation.
Lengefeld et al. reveal how yeast cells distinguish between newly synthesized and pre-existing spindle pole bodies to enable their asymmetric segregation, through a mechanism involving Swe1, Kin3 and NuA4.
Pitulescu et al. and Hasan et al. show that Dll4–Notch signalling in endothelial tip cells regulates angiogenesis through control of artery formation, linking sprouting angiogenesis and artery formation.
Zhou et al. show that in the context of AML1-ETO-driven leukaemia, AES and DDX21 induce small nucleolar RNA (snoRNA)–ribonucleoprotein (RNP) formation and this is important for self-renewal of leukaemic cells.
Ban et al. show that optic atrophy 1 (OPA1) and cardiolipin mediate mitochondrial fusion. In contrast, a homotypic trans-OPA1 interaction independent of cardiolipin mediates membrane tethering to form mitochondrial cristae.
Wang et al. show that glucose deprivation causes AMPK-dependent phosphorylation of fumarase leading to ATF2 binding and gene transcription for cell cycle arrest. In cancer cells O-GlcNAcylation of fumarase blocks ATF2 binding to allow proliferation.
Kronenberg et al. develop a system to record cell–substrate interactions allowing the measurement of horizontal and vertical forces at high resolution, and demonstrate its use by monitoring podosome protrusion and other cell behaviours.
Graf et al. demonstrate that Pramel7 maintains ground-state pluripotency by repressing DNA methylation through proteasomal degradation of UHRF1, thus linking the proteasome and epigenetics with cell fate regulation.
Wang et al. show that lipid-induced ROS lead to ACAT2 stabilization by oxidizing a cysteine residue, thereby preventing its ubiquitylation and ACAT2 degradation. They further show that ACAT2 stabilization improves lipotoxicity and insulin resistance.
Mierzwa et al. show that ESCRT-III subunit turnover at the cell midbody is driven by Vps4. Rapid turnover sustains the net growth of ESCRT-III assemblies in the presence of inhibitory Vps2 and Vps24 subunits.