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It is generally accepted that protein function depends on a defined 3D structure, with unfolding and aggregation dealing a final blow to functionality. A study now shows that the regulated exposure of an unstructured region in yeast pyruvate kinase triggers reversible aggregation to preserve protein function under stress.
Recycling from endosomes to the plasma membrane is an important step in cell homeostasis. The retromer/SNX27/WASH complex recycles numerous receptors, but key ones are still unaccounted for. Now a related conserved heterotrimer, called retriever, has been identified that, together with SNX17, the CCC complex and WASH, mediates the recycling of α5β1 integrins.
Cancer cells preferentially metastasize to certain organs. A study in mouse models of breast cancer shows that the DKK1 negative regulator of WNT signalling inhibits tropism to the lung, but enhances tropism to the bone due to the differential regulation of canonical and non-canonical WNT signalling in the two microenvironments.
During muscle development, nuclei travel from the centre of the myofibre to the periphery, a process defective in certain diseases. A new study reveals that this movement is due to centripetal forces imposed on nuclei by the crosslinking and contraction of myofibrils.
The cytokine tumour necrosis factor (TNF) and the toll-like receptors (TLRs) coordinate immune responses by activating inflammatory transcriptional programs, but these signals can also trigger cell death. Recent studies identify the MAP kinase substrate MK2 as a key player in determining whether cells live or die in response to TNF and TLR signalling.
Ganuza et al. track newly specified blood progenitors in the dorsal aorta of the mouse embryo and demonstrate that they are polyclonal in origin and that hundreds of mesodermal, endothelial and blood precursors establish lifelong haematopoiesis.
Anderson et al. show that LIF, ActA and Wnt support self-renewal in both pluripotent and endodermal cells. Upon removal of insulin, they induce differentiation of naive PSCs into extra-embryonic primitive endoderm and primed PSCs into definitive endoderm.
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.
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.
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.
Wu et al. show that prosurvival BCL-2 proteins disrupt SUFU repression of GLI activity, leading to GLI target gene expression. BH3 mimetics disable GLI transcriptional activity driven by HH pathway mutations.
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.
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.
Wu et al. find that tumour hypoxic conditions increase miR25/93 levels, which via targeting Ncoa3 downregulate the expression of the innate immune regulator cGAS, thus allowing escape of the anti-tumour immune response.
