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Journal Cover Nature
  [SJR: 21.936]   [H-I: 948]   [4180 followers]  Follow
    
   Full-text available via subscription Subscription journal
   ISSN (Print) 0028-0836 - ISSN (Online) 1476-4687
   Published by NPG Homepage  [135 journals]
  • Science must examine the future of work
    • Pages: 301 - 302
      Abstract: As automation changes employment, researchers should gather the evidence to help map the implications.
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-18
      DOI: 10.1038/550301b
      Issue No: Vol. 550, No. 7676 (2017)
       
  • Eye in the sky offers clearest vision of Earth
    • Pages: 301 - 301
      Abstract: The world’s latest carbon-monitoring satellite has advanced our understanding of how the planet functions. US politicians should take note.
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-16
      DOI: 10.1038/550301a
      Issue No: Vol. 550, No. 7676 (2017)
       
  • Blue is in the eye of the bee-holder
    • Pages: 302 - 302
      Abstract: Flowers have evolved an ingenious way to attract pollinators.
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-18
      DOI: 10.1038/550302a
      Issue No: Vol. 550, No. 7676 (2017)
       
  • Give researchers a lifetime word limit
    • Authors: Brian C. Martinson
      Pages: 303 - 303
      Abstract: Brian C. Martinson imagines how rationing the number of publications a scientist could put out might improve the scientific literature.
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-17
      DOI: 10.1038/550303a
      Issue No: Vol. 550, No. 7676 (2017)
       
  • Epic star collision, asteroid fly-by and journal resignations
    • Pages: 306 - 307
      Abstract: The week in science: 13–19 October 2017.
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-18
      DOI: 10.1038/550306a
      Issue No: Vol. 550, No. 7676 (2017)
       
  • Colliding stars spark rush to solve cosmic mysteries
    • Authors: Davide Castelvecchi
      Pages: 309 - 310
      Abstract: Stellar collision confirms theoretical predictions about the periodic table.
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-16
      DOI: 10.1038/550309a
      Issue No: Vol. 550, No. 7676 (2017)
       
  • Japanese research leaders warn about national science decline
    • Authors: Nicky Phillips
      Pages: 310 - 311
      Abstract: Concern mounts over budget cuts and other changes that undermine basic science.
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-17
      DOI: 10.1038/550310a
      Issue No: Vol. 550, No. 7676 (2017)
       
  • Trump EPA begins push to overturn Obama-era climate regulation
    • Authors: Jeff Tollefson
      Pages: 311 - 311
      Abstract: The agency's plan to reverse limits on greenhouse-gas emissions is likely to draw legal challenges.
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-10
      DOI: 10.1038/nature.2017.22813
      Issue No: Vol. 550, No. 7676 (2017)
       
  • New definitions of scientific units are on the horizon
    • Authors: Elizabeth Gibney
      Pages: 312 - 313
      Abstract: Metrologists are poised to change how scientists measure the Universe.
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-18
      DOI: 10.1038/550312a
      Issue No: Vol. 550, No. 7676 (2017)
       
  • FDA advisers back gene therapy for rare form of blindness
    • Authors: Heidi Ledford
      Pages: 314 - 314
      Abstract: Therapy that targets disease-causing mutations could become the first of its kind approved for use in the United States.
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-12
      DOI: 10.1038/nature.2017.22819
      Issue No: Vol. 550, No. 7676 (2017)
       
  • The future of work
    • Pages: 315 - 315
      Abstract: Digital technologies are upending the workforce. The right research can tell us how.
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-18
      DOI: 10.1038/550315a
      Issue No: Vol. 550, No. 7676 (2017)
       
  • Lessons from history for the future of work
    • Authors: Robert C. Allen
      Pages: 321 - 324
      Abstract: Global comparisons of previous social and economic upheavals suggest that what is to come depends on where you are now, argues Robert C. Allen.
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-18
      DOI: 10.1038/550321a
      Issue No: Vol. 550, No. 7676 (2017)
       
  • Reboot for the AI revolution
    • Authors: Yuval Noah Harari
      Pages: 324 - 327
      Abstract: As artificial intelligence puts many out of work, we must forge new economic, social and educational systems, argues Yuval Noah Harari.
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-17
      DOI: 10.1038/550324a
      Issue No: Vol. 550, No. 7676 (2017)
       
  • The second Renaissance
    • Authors: Ian Goldin
      Pages: 327 - 329
      Abstract: Ian Goldin calls on scientists to help society to weather the disruptive transformations afoot.
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-18
      DOI: 10.1038/550327a
      Issue No: Vol. 550, No. 7676 (2017)
       
  • Archaeology: The wonder of the pyramids
    • Authors: Andrew Robinson
      Pages: 330 - 331
      Abstract: Andrew Robinson enjoys a volume rounding up research on the complex at Giza, Egypt.
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-18
      DOI: 10.1038/550330a
      Issue No: Vol. 550, No. 7676 (2017)
       
  • Books in brief
    • Authors: Barbara Kiser
      Pages: 331 - 331
      Abstract: Barbara Kiser reviews five of the week's best science picks.
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-18
      DOI: 10.1038/550331a
      Issue No: Vol. 550, No. 7676 (2017)
       
  • History: Five millennia of Indian science
    • Authors: James Poskett
      Pages: 332 - 332
      Abstract: James Poskett applauds a show celebrating discovery on the subcontinent, from zero to the boson.
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-18
      DOI: 10.1038/550332a
      Issue No: Vol. 550, No. 7676 (2017)
       
  • Federal funding: Stifled by budgets, not irrelevance
    • Authors: Thomas O. Baldwin
      Pages: 333 - 333
      Abstract: Daniel Sarewitz constructs a stereotype of scientists who are left to their own devices and whose research is disconnected from potential applications (Nature547, 139; 10.1038/547139a2017). As president of the Federation of American Societies for Experimental Biology (FASEB), I argue
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-18
      DOI: 10.1038/550333a
      Issue No: Vol. 550, No. 7676 (2017)
       
  • Ornithology: Danish dairy farmer delivers data coup
    • Authors: Tony Fox, Henning Heldbjerg
      Pages: 333 - 333
      Abstract: Neither the name Peder V. Thellesen nor the Danish Ornithological Society Journal will resonate with most Nature readers. In a striking example of citizen science, the Danish journal has just published 45 years of Thellesen's breeding data from his studies of starlings (
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-18
      DOI: 10.1038/550333b
      Issue No: Vol. 550, No. 7676 (2017)
       
  • Open data: Spot data glitches before publication
    • Authors: Noah F. Greenwald, Pratiti Bandopadhayay, Rameen Beroukhim
      Pages: 333 - 333
      Abstract: Deposition of raw data into publicly available databases — now a condition of publication in many journals (Nature537, 138; 10.1038/537138a2016) — needs to involve more than just another checkbox for the senior author. Before accepting a manuscript, journals should
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-18
      DOI: 10.1038/550333c
      Issue No: Vol. 550, No. 7676 (2017)
       
  • PhD students: living wage key to diversity
    • Authors: Larissa K. Barber, Nicholas A. Barber, Holly P. Jones
      Pages: 333 - 333
      Abstract: In our view, your report on side jobs for scientists paints a naive and insensitive picture of the financial and social realities facing many graduate students and other early-career researchers (Nature549, 297–299; 10.1038/nj7671-297a2017). For a group already
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-18
      DOI: 10.1038/550333d
      Issue No: Vol. 550, No. 7676 (2017)
       
  • PhD students: side jobs are no solution
    • Authors: Therice Morris
      Pages: 333 - 333
      Abstract: As a graduate student at a US university, I object strongly to any implication that PhD students should take other jobs on top of their already demanding research (Nature549, 297–299; 10.1038/nj7671-297a2017). That is not, nor should it
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-18
      DOI: 10.1038/550333e
      Issue No: Vol. 550, No. 7676 (2017)
       
  • Artificial intelligence: Learning to play Go from scratch
    • Authors: Satinder Singh, Andy Okun, Andrew Jackson
      Pages: 336 - 337
      Abstract: An artificial-intelligence program called AlphaGo Zero has mastered the game of Go without any human data or guidance. A computer scientist and two members of the American Go Association discuss the implications. See Article p.354
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-18
      DOI: 10.1038/550336a
      Issue No: Vol. 550, No. 7676 (2017)
       
  • Cancer treatment: Bacterial snack attack deactivates a drug
    • Authors: Christian Jobin
      Pages: 337 - 339
      Abstract: Tumour cells can develop intrinsic adaptations that make them less susceptible to chemotherapy. It emerges that extrinsic bacterial action can also enable tumour cells to escape the effects of drug treatment.
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-18
      DOI: 10.1038/550337a
      Issue No: Vol. 550, No. 7676 (2017)
       
  • 50 & 100 Years Ago
    • Pages: 339 - 339
      Abstract: 50 Years AgoOur society is crimogenic, in that our social structure produces most crime, which must therefore be regarded as one “normal” response to social stimuli. For an adequate understanding of its causation, and of appropriate remedial action, we must therefore rely primarily on
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-18
      DOI: 10.1038/550339b
      Issue No: Vol. 550, No. 7676 (2017)
       
  • Computer science: Data analysis meets quantum physics
    • Authors: Steven Schramm
      Pages: 339 - 340
      Abstract: A technique that combines machine learning and quantum computing has been used to identify the particles known as Higgs bosons. The method could find applications in many areas of science. See Letter p.375
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-18
      DOI: 10.1038/550339a
      Issue No: Vol. 550, No. 7676 (2017)
       
  • Cancer biology: Genome jail-break triggers lockdown
    • Authors: Neil T. Umbreit, David Pellman
      Pages: 340 - 341
      Abstract: A pro-inflammatory response, the senescence-associated secretory phenotype, can affect development, ageing and cancer. It emerges that one trigger for this response is the presence of DNA in the cytoplasm. See Letter p.402
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-04
      DOI: 10.1038/nature24146
      Issue No: Vol. 550, No. 7676 (2017)
       
  • Biochemistry: Complex assistance for DNA invasion
    • Authors: Petr Cejka
      Pages: 342 - 343
      Abstract: Repair of broken DNA is vital for genome stability and to prevent the development of cancer. Research shows how the tumour-suppressor protein BRCA1 promotes a DNA-repair pathway called homologous recombination. See Article p.360
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-04
      DOI: 10.1038/nature24149
      Issue No: Vol. 550, No. 7676 (2017)
       
  • Neurobiology: Domains to the rescue for Rett syndrome
    • Authors: Anne E. West
      Pages: 343 - 344
      Abstract: Rett syndrome is a brain disorder caused by disrupted forms of the protein MECP2, but how MECP2 loss affects the brain is unknown. A mouse study now implicates key domains of the protein and offers therapeutic insights. See Letter p.398
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-11
      DOI: 10.1038/nature24151
      Issue No: Vol. 550, No. 7676 (2017)
       
  • DNA sequencing at 40: past, present and future
    • Authors: Jay Shendure, Shankar Balasubramanian, George M. Church, Walter Gilbert, Jane Rogers, Jeffery A. Schloss, Robert H. Waterston
      Pages: 345 - 353
      Abstract: This review commemorates the 40th anniversary of DNA sequencing, a period in which we have already witnessed multiple technological revolutions and a growth in scale from a few kilobases to the first human genome, and now to millions of human and a myriad of other
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-11
      DOI: 10.1038/nature24286
      Issue No: Vol. 550, No. 7676 (2017)
       
  • Mastering the game of Go without human knowledge
    • Authors: David Silver, Julian Schrittwieser, Karen Simonyan, Ioannis Antonoglou, Aja Huang, Arthur Guez, Thomas Hubert, Lucas Baker, Matthew Lai, Adrian Bolton, Yutian Chen, Timothy Lillicrap, Fan Hui, Laurent Sifre, George van den Driessche, Thore Graepel, Demis Hassabis
      Pages: 354 - 359
      Abstract: A long-standing goal of artificial intelligence is an algorithm that learns, tabula rasa, superhuman proficiency in challenging domains. Recently, AlphaGo became the first program to defeat a world champion in the game of Go. The tree search in AlphaGo evaluated positions and selected moves
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-18
      DOI: 10.1038/nature24270
      Issue No: Vol. 550, No. 7676 (2017)
       
  • BRCA1–BARD1 promotes RAD51-mediated homologous DNA pairing
    • Authors: Weixing Zhao, Justin B. Steinfeld, Fengshan Liang, Xiaoyong Chen, David G. Maranon, Chu Jian Ma, Youngho Kwon, Timsi Rao, Weibin Wang, Chen Sheng, Xuemei Song, Yanhong Deng, Judit Jimenez-Sainz, Lucy Lu, Ryan B. Jensen, Yong Xiong, Gary M. Kupfer, Claudia Wiese, Eric C. Greene, Patrick Sung
      Pages: 360 - 365
      Abstract: The tumour suppressor complex BRCA1–BARD1 functions in the repair of DNA double-stranded breaks by homologous recombination. During this process, BRCA1–BARD1 facilitates the nucleolytic resection of DNA ends to generate a single-stranded template for the recruitment of another tumour suppressor complex, BRCA2–PALB2, and the recombinase RAD51.
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-04
      DOI: 10.1038/nature24060
      Issue No: Vol. 550, No. 7676 (2017)
       
  • Human TRPML1 channel structures in open and closed conformations
    • Authors: Philip Schmiege, Michael Fine, Günter Blobel, Xiaochun Li
      Pages: 366 - 370
      Abstract: Transient receptor potential mucolipin 1 (TRPML1) is a Ca2+-releasing cation channel that mediates the calcium signalling and homeostasis of lysosomes. Mutations in TRPML1 lead to mucolipidosis type IV, a severe lysosomal storage disorder. Here we report two electron cryo-microscopy structures of full-length human
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-11
      DOI: 10.1038/nature24036
      Issue No: Vol. 550, No. 7676 (2017)
       
  • A parts-per-billion measurement of the antiproton magnetic moment
    • Authors: C. Smorra, S. Sellner, M. J. Borchert, J. A. Harrington, T. Higuchi, H. Nagahama, T. Tanaka, A. Mooser, G. Schneider, M. Bohman, K. Blaum, Y. Matsuda, C. Ospelkaus, W. Quint, J. Walz, Y. Yamazaki, S. Ulmer
      Pages: 371 - 374
      Abstract: Precise comparisons of the fundamental properties of matter–antimatter conjugates provide sensitive tests of charge–parity–time (CPT) invariance, which is an important symmetry that rests on basic assumptions of the standard model of particle physics. Experiments on mesons, leptons and baryons have compared different properties of matter–antimatter conjugates with fractional uncertainties at the parts-per-billion level or better. One specific quantity, however, has so far only been known to a fractional uncertainty at the parts-per-million level: the magnetic moment of the antiproton, . The extraordinary difficulty in measuring with high precision is caused by its intrinsic smallness; for example, it is 660 times smaller than the magnetic moment of the positron. Here we report a high-precision measurement of in units of the nuclear magneton μN with a fractional precision of 1.5 parts per billion (68% confidence level). We use a two-particle spectroscopy method in an advanced cryogenic multi-Penning trap system. Our result  = −2.7928473441(42)μN (where the number in parentheses represents the 68% confidence interval on the last digits of the value) improves the precision of the previous best measurement by a factor of approximately 350. The measured value is consistent with the proton magnetic moment, μp = 2.792847350(9)μN, and is in agreement with CPT invariance. Consequently, this measurement constrains the magnitude of certain CPT-violating effects to below 1.8 × 10−24 gigaelectronvolts, and a possible splitting of the proton–antiproton magnetic moments by CPT-odd dimension-five interactions to below 6 × 10−12 Bohr magnetons.
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-18
      DOI: 10.1038/nature24048
      Issue No: Vol. 550, No. 7676 (2017)
       
  • Solving a Higgs optimization problem with quantum annealing for machine
           learning
    • Authors: Alex Mott, Joshua Job, Jean-Roch Vlimant, Daniel Lidar, Maria Spiropulu
      Pages: 375 - 379
      Abstract: The discovery of Higgs-boson decays in a background of standard-model processes was assisted by machine learning methods. The classifiers used to separate signals such as these from background are trained using highly unerring but not completely perfect simulations of the physical processes involved, often resulting in incorrect labelling of background processes or signals (label noise) and systematic errors. Here we use quantum and classical annealing (probabilistic techniques for approximating the global maximum or minimum of a given function) to solve a Higgs-signal-versus-background machine learning optimization problem, mapped to a problem of finding the ground state of a corresponding Ising spin model. We build a set of weak classifiers based on the kinematic observables of the Higgs decay photons, which we then use to construct a strong classifier. This strong classifier is highly resilient against overtraining and against errors in the correlations of the physical observables in the training data. We show that the resulting quantum and classical annealing-based classifier systems perform comparably to the state-of-the-art machine learning methods that are currently used in particle physics. However, in contrast to these methods, the annealing-based classifiers are simple functions of directly interpretable experimental parameters with clear physical meaning. The annealer-trained classifiers use the excited states in the vicinity of the ground state and demonstrate some advantage over traditional machine learning methods for small training datasets. Given the relative simplicity of the algorithm and its robustness to error, this technique may find application in other areas of experimental particle physics, such as real-time decision making in event-selection problems and classification in neutrino physics.
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-18
      DOI: 10.1038/nature24047
      Issue No: Vol. 550, No. 7676 (2017)
       
  • Ion sieving in graphene oxide membranes via cationic control of interlayer
           spacing
    • Authors: Liang Chen, Guosheng Shi, Jie Shen, Bingquan Peng, Bowu Zhang, Yuzhu Wang, Fenggang Bian, Jiajun Wang, Deyuan Li, Zhe Qian, Gang Xu, Gongping Liu, Jianrong Zeng, Lijuan Zhang, Yizhou Yang, Guoquan Zhou, Minghong Wu, Wanqin Jin, Jingye Li, Haiping Fang
      Pages: 380 - 383
      Abstract: Graphene oxide membranes—partially oxidized, stacked sheets of graphene—can provide ultrathin, high-flux and energy-efficient membranes for precise ionic and molecular sieving in aqueous solution. These materials have shown potential in a variety of applications, including water desalination and purification, gas and ion separation, biosensors, proton conductors, lithium-based batteries and super-capacitors. Unlike the pores of carbon nanotube membranes, which have fixed sizes, the pores of graphene oxide membranes—that is, the interlayer spacing between graphene oxide sheets (a sheet is a single flake inside the membrane)—are of variable size. Furthermore, it is difficult to reduce the interlayer spacing sufficiently to exclude small ions and to maintain this spacing against the tendency of graphene oxide membranes to swell when immersed in aqueous solution. These challenges hinder the potential ion filtration applications of graphene oxide membranes. Here we demonstrate cationic control of the interlayer spacing of graphene oxide membranes with ångström precision using K+, Na+, Ca2+, Li+ or Mg2+ ions. Moreover, membrane spacings controlled by one type of cation can efficiently and selectively exclude other cations that have larger hydrated volumes. First-principles calculations and ultraviolet absorption spectroscopy reveal that the location of the most stable cation adsorption is where oxide groups and aromatic rings coexist. Previous density functional theory computations show that other cations (Fe2+, Co2+, Cu2+, Cd2+, Cr2+ and Pb2+) should have a much stronger cation–π interaction with the graphene sheet than Na+ has, suggesting that other ions could be used to produce a wider range of interlayer spacings.
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-09
      DOI: 10.1038/nature24044
      Issue No: Vol. 550, No. 7676 (2017)
       
  • Organic long persistent luminescence
    • Authors: Ryota Kabe, Chihaya Adachi
      Pages: 384 - 387
      Abstract: Long persistent luminescence (LPL) materials—widely commercialized as ‘glow-in-the-dark’ paints—store excitation energy in excited states that slowly release this energy as light. At present, most LPL materials are based on an inorganic system of strontium aluminium oxide (SrAl2O4) doped with europium and dysprosium, and exhibit emission for more than ten hours. However, this system requires rare elements and temperatures higher than 1,000 degrees Celsius during fabrication, and light scattering by SrAl2O4 powders limits the transparency of LPL paints. Here we show that an organic LPL (OLPL) system of two simple organic molecules that is free from rare elements and easy to fabricate can generate emission that lasts for more than one hour at room temperature. Previous organic systems, which were based on two-photon ionization, required high excitation intensities and low temperatures. By contrast, our OLPL system—which is based on emission from excited complexes (exciplexes) upon the recombination of long-lived charge-separated states—can be excited by a standard white LED light source and generate long emission even at temperatures above 100 degrees Celsius. This OLPL system is transparent, soluble, and potentially flexible and colour-tunable, opening new applications for LPL in large-area and flexible paints, biomarkers, fabrics, and windows. Moreover, the study of long-lived charge separation in this system should advance understanding of a wide variety of organic semiconductor devices.
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-02
      DOI: 10.1038/nature24010
      Issue No: Vol. 550, No. 7676 (2017)
       
  • Social behaviour shapes hypothalamic neural ensemble representations of
           conspecific sex
    • Authors: Ryan Remedios, Ann Kennedy, Moriel Zelikowsky, Benjamin F. Grewe, Mark J. Schnitzer, David J. Anderson
      Pages: 388 - 392
      Abstract: All animals possess a repertoire of innate (or instinctive) behaviours, which can be performed without training. Whether such behaviours are mediated by anatomically distinct and/or genetically specified neural pathways remains unknown. Here we report that neural representations within the mouse hypothalamus, that underlie innate social behaviours, are shaped by social experience. Oestrogen receptor 1-expressing (Esr1+) neurons in the ventrolateral subdivision of the ventromedial hypothalamus (VMHvl) control mating and fighting in rodents. We used microendoscopy to image Esr1+ neuronal activity in the VMHvl of male mice engaged in these social behaviours. In sexually and socially experienced adult males, divergent and characteristic neural ensembles represented male versus female conspecifics. However, in inexperienced adult males, male and female intruders activated overlapping neuronal populations. Sex-specific neuronal ensembles gradually separated as the mice acquired social and sexual experience. In mice permitted to investigate but not to mount or attack conspecifics, ensemble divergence did not occur. However, 30 minutes of sexual experience with a female was sufficient to promote the separation of male and female ensembles and to induce an attack response 24 h later. These observations uncover an unexpected social experience-dependent component to the formation of hypothalamic neural assemblies controlling innate social behaviours. More generally, they reveal plasticity and dynamic coding in an evolutionarily ancient deep subcortical structure that is traditionally viewed as a ‘hard-wired’ system.
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-18
      DOI: 10.1038/nature23885
      Issue No: Vol. 550, No. 7676 (2017)
       
  • Establishment of mouse expanded potential stem cells
    • Authors: Jian Yang, David J. Ryan, Wei Wang, Jason Cheuk-Ho Tsang, Guocheng Lan, Hideki Masaki, Xuefei Gao, Liliana Antunes, Yong Yu, Zhexin Zhu, Juexuan Wang, Aleksandra A. Kolodziejczyk, Lia S. Campos, Cui Wang, Fengtang Yang, Zhen Zhong, Beiyuan Fu, Melanie A. Eckersley-Maslin, Michael Woods, Yosuke Tanaka, Xi Chen, Adam C. Wilkinson, James Bussell, Jacqui White, Ramiro Ramirez-Solis, Wolf Reik, Berthold Göttgens, Sarah A. Teichmann, Patrick P. L. Tam, Hiromitsu Nakauchi, Xiangang Zou, Liming Lu, Pentao Liu
      Pages: 393 - 397
      Abstract: Mouse embryonic stem cells derived from the epiblast contribute to the somatic lineages and the germline but are excluded from the extra-embryonic tissues that are derived from the trophectoderm and the primitive endoderm upon reintroduction to the blastocyst. Here we report that cultures of expanded potential stem cells can be established from individual eight-cell blastomeres, and by direct conversion of mouse embryonic stem cells and induced pluripotent stem cells. Remarkably, a single expanded potential stem cell can contribute both to the embryo proper and to the trophectoderm lineages in a chimaera assay. Bona fide trophoblast stem cell lines and extra-embryonic endoderm stem cells can be directly derived from expanded potential stem cells in vitro. Molecular analyses of the epigenome and single-cell transcriptome reveal enrichment for blastomere-specific signature and a dynamic DNA methylome in expanded potential stem cells. The generation of mouse expanded potential stem cells highlights the feasibility of establishing expanded potential stem cells for other mammalian species.
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-11
      DOI: 10.1038/nature24052
      Issue No: Vol. 550, No. 7676 (2017)
       
  • Radically truncated MeCP2 rescues Rett syndrome-like neurological defects
    • Authors: Rebekah Tillotson, Jim Selfridge, Martha V. Koerner, Kamal K. E. Gadalla, Jacky Guy, Dina De Sousa, Ralph D. Hector, Stuart R. Cobb, Adrian Bird
      Pages: 398 - 401
      Abstract: Heterozygous mutations in the X-linked MECP2 gene cause the neurological disorder Rett syndrome. The methyl-CpG-binding protein 2 (MeCP2) protein is an epigenetic reader whose binding to chromatin primarily depends on 5-methylcytosine. Functionally, MeCP2 has been implicated in several cellular processes on the basis of its reported interaction with more than 40 binding partners, including transcriptional co-repressors (for example, the NCoR/SMRT complex), transcriptional activators, RNA, chromatin remodellers, microRNA-processing proteins and splicing factors. Accordingly, MeCP2 has been cast as a multi-functional hub that integrates diverse processes that are essential in mature neurons. At odds with the concept of broad functionality, missense mutations that cause Rett syndrome are concentrated in two discrete clusters coinciding with interaction sites for partner macromolecules: the methyl-CpG binding domain and the NCoR/SMRT interaction domain. Here we test the hypothesis that the single dominant function of MeCP2 is to physically connect DNA with the NCoR/SMRT complex, by removing almost all amino-acid sequences except the methyl-CpG binding and NCoR/SMRT interaction domains. We find that mice expressing truncated MeCP2 lacking both the N- and C-terminal regions (approximately half of the native protein) are phenotypically near-normal; and those expressing a minimal MeCP2 additionally lacking a central domain survive for over one year with only mild symptoms. This minimal protein is able to prevent or reverse neurological symptoms when introduced into MeCP2-deficient mice by genetic activation or virus-mediated delivery to the brain. Thus, despite evolutionary conservation of the entire MeCP2 protein sequence, the DNA and co-repressor binding domains alone are sufficient to avoid Rett syndrome-like defects and may therefore have therapeutic utility.
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-11
      DOI: 10.1038/nature24058
      Issue No: Vol. 550, No. 7676 (2017)
       
  • Cytoplasmic chromatin triggers inflammation in senescence and cancer
    • Authors: Zhixun Dou, Kanad Ghosh, Maria Grazia Vizioli, Jiajun Zhu, Payel Sen, Kirk J. Wangensteen, Johayra Simithy, Yemin Lan, Yanping Lin, Zhuo Zhou, Brian C. Capell, Caiyue Xu, Mingang Xu, Julia E. Kieckhaefer, Tianying Jiang, Michal Shoshkes-Carmel, K. M. Ahasan Al Tanim, Glen N. Barber, John T. Seykora, Sarah E. Millar, Klaus H. Kaestner, Benjamin A. Garcia, Peter D. Adams, Shelley L. Berger
      Pages: 402 - 406
      Abstract: Chromatin is traditionally viewed as a nuclear entity that regulates gene expression and silencing. However, we recently discovered the presence of cytoplasmic chromatin fragments that pinch off from intact nuclei of primary cells during senescence, a form of terminal cell-cycle arrest associated with pro-inflammatory responses. The functional significance of chromatin in the cytoplasm is unclear. Here we show that cytoplasmic chromatin activates the innate immunity cytosolic DNA-sensing cGAS–STING (cyclic GMP–AMP synthase linked to stimulator of interferon genes) pathway, leading both to short-term inflammation to restrain activated oncogenes and to chronic inflammation that associates with tissue destruction and cancer. The cytoplasmic chromatin–cGAS–STING pathway promotes the senescence-associated secretory phenotype in primary human cells and in mice. Mice deficient in STING show impaired immuno-surveillance of oncogenic RAS and reduced tissue inflammation upon ionizing radiation. Furthermore, this pathway is activated in cancer cells, and correlates with pro-inflammatory gene expression in human cancers. Overall, our findings indicate that genomic DNA serves as a reservoir to initiate a pro-inflammatory pathway in the cytoplasm in senescence and cancer. Targeting the cytoplasmic chromatin-mediated pathway may hold promise in treating inflammation-related disorders.
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-04
      DOI: 10.1038/nature24050
      Issue No: Vol. 550, No. 7676 (2017)
       
  • Enhanced proofreading governs CRISPR–Cas9 targeting accuracy
    • Authors: Janice S. Chen, Yavuz S. Dagdas, Benjamin P. Kleinstiver, Moira M. Welch, Alexander A. Sousa, Lucas B. Harrington, Samuel H. Sternberg, J. Keith Joung, Ahmet Yildiz, Jennifer A. Doudna
      Pages: 407 - 410
      Abstract: The RNA-guided CRISPR–Cas9 nuclease from Streptococcus pyogenes (SpCas9) has been widely repurposed for genome editing. High-fidelity (SpCas9-HF1) and enhanced specificity (eSpCas9(1.1)) variants exhibit substantially reduced off-target cleavage in human cells, but the mechanism of target discrimination and the potential to further improve fidelity are unknown. Here, using single-molecule Förster resonance energy transfer experiments, we show that both SpCas9-HF1 and eSpCas9(1.1) are trapped in an inactive state when bound to mismatched targets. We find that a non-catalytic domain within Cas9, REC3, recognizes target complementarity and governs the HNH nuclease to regulate overall catalytic competence. Exploiting this observation, we design a new hyper-accurate Cas9 variant (HypaCas9) that demonstrates high genome-wide specificity without compromising on-target activity in human cells. These results offer a more comprehensive model to rationalize and modify the balance between target recognition and nuclease activation for precision genome editing.
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-09-20
      DOI: 10.1038/nature24268
      Issue No: Vol. 550, No. 7676 (2017)
       
  • Cryo-electron microscopy structure of the lysosomal calcium-permeable
           channel TRPML3
    • Authors: Marscha Hirschi, Mark A. Herzik Jr, Jinhong Wie, Yang Suo, William F. Borschel, Dejian Ren, Gabriel C. Lander, Seok-Yong Lee
      Pages: 411 - 414
      Abstract: The modulation of ion channel activity by lipids is increasingly recognized as a fundamental component of cellular signalling. The transient receptor potential mucolipin (TRPML) channel family belongs to the TRP superfamily and is composed of three members: TRPML1–TRPML3. TRPMLs are the major Ca2+-permeable channels on late endosomes and lysosomes (LEL). They regulate the release of Ca2+ from organelles, which is important for various physiological processes, including organelle trafficking and fusion. Loss-of-function mutations in the MCOLN1 gene, which encodes TRPML1, cause the neurodegenerative lysosomal storage disorder mucolipidosis type IV, and a gain-of-function mutation (Ala419Pro) in TRPML3 gives rise to the varitint–waddler (Va) mouse phenotype. Notably, TRPML channels are activated by the low-abundance and LEL-enriched signalling lipid phosphatidylinositol-3,5-bisphosphate (PtdIns(3,5)P2), whereas other phosphoinositides such as PtdIns(4,5)P2, which is enriched in plasma membranes, inhibit TRPMLs. Conserved basic residues at the N terminus of the channel are important for activation by PtdIns(3,5)P2 and inhibition by PtdIns(4,5)P2. However, owing to a lack of structural information, the mechanism by which TRPML channels recognize PtdIns(3,5)P2 and increase their Ca2+ conductance remains unclear. Here we present the cryo-electron microscopy (cryo-EM) structure of a full-length TRPML3 channel from the common marmoset (Callithrix jacchus) at an overall resolution of 2.9 Å. Our structure reveals not only the molecular basis of ion conduction but also the unique architecture of TRPMLs, wherein the voltage sensor-like domain is linked to the pore via a cytosolic domain that we term the mucolipin domain. Combined with functional studies, these data suggest that the mucolipin domain is responsible for PtdIns(3,5)P2 binding and subsequent channel activation, and that it acts as a ‘gating pulley’ for lipid-dependent TRPML gating.
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-11
      DOI: 10.1038/nature24055
      Issue No: Vol. 550, No. 7676 (2017)
       
  • Structure of mammalian endolysosomal TRPML1 channel in nanodiscs
    • Authors: Qingfeng Chen, Ji She, Weizhong Zeng, Jiangtao Guo, Haoxing Xu, Xiao-chen Bai, Youxing Jiang
      Pages: 415 - 418
      Abstract: Transient receptor potential mucolipin 1 (TRPML1) is a cation channel located within endosomal and lysosomal membranes. Ubiquitously expressed in mammalian cells, its loss-of-function mutations are the direct cause of type IV mucolipidosis, an autosomal recessive lysosomal storage disease. Here we present the single-particle electron cryo-microscopy structure of the mouse TRPML1 channel embedded in nanodiscs. Combined with mutagenesis analysis, the TRPML1 structure reveals that phosphatidylinositol-3,5-bisphosphate (PtdIns(3,5)P2) binds to the N terminus of the channel—distal from the pore—and the helix–turn–helix extension between segments S2 and S3 probably couples ligand binding to pore opening. The tightly packed selectivity filter contains multiple ion-binding sites, and the conserved acidic residues form the luminal Ca2+-blocking site that confers luminal pH and Ca2+ modulation on channel conductance. A luminal linker domain forms a fenestrated canopy atop the channel, providing several luminal ion passages to the pore and creating a negative electrostatic trap, with a preference for divalent cations, at the luminal entrance. The structure also reveals two equally distributed S4–S5 linker conformations in the closed channel, suggesting an S4–S5 linker-mediated PtdInsP2 gating mechanism among TRPML channels.
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-11
      DOI: 10.1038/nature24035
      Issue No: Vol. 550, No. 7676 (2017)
       
  • Flexible working: Science in the gig economy
    • Authors: Roberta Kwok
      Pages: 419 - 421
      Abstract: Will the future of research rely on independent workers who perform short-term jobs' Labour researchers and freelance scientists share their views.
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-18
      DOI: 10.1038/nj7676-419a
      Issue No: Vol. 550, No. 7676 (2017)
       
  • Trade talk: Habitat helper
    • Trade talk: Habitat helper

      Nature 550, 7676 (2017). doi:10.1038/nj7676-421a

      Author: Sarah Boon

      Nature 550, 7676 (2017)2017-10-18
      DOI: 10.1038/nj7676-421a
      Issue No: Vol. 550, No. 7676 (2017)
       
  • Breaking and entering
    • Authors: Hall Jameson
      Pages: 424 - 424
      Abstract: Escape is not an option.
      Citation: Nature 550, 7676 (2017)
      PubDate: 2017-10-18
      DOI: 10.1038/550424a
      Issue No: Vol. 550, No. 7676 (2017)
       
  • Amyotrophic lateral sclerosis
    • Amyotrophic lateral sclerosis

      Nature. doi:10.1038/550S105a

      Author: Brian Owens

      Nature2017-10-18
      DOI: 10.1038/550S105a
       
  • Genetics: The hexanucleotide hex
    • Authors: Elie Dolgin
      Abstract: For years, researchers missed the most common genetic cause of ALS. Now they're on an accelerated track to treat it.
      Citation: Nature
      PubDate: 2017-10-18
      DOI: 10.1038/550S106a
       
  • Non-Familial ALS: A tangled web
    • Authors: Carolyn Brown
      Abstract: Research ranging in scale from cells to populations is rapidly closing in on what goes awry in the body in 'non-familial' ALS, and what environmental factors might contribute.
      Citation: Nature
      PubDate: 2017-10-18
      DOI: 10.1038/550S109a
       
  • Perspective: Don't keep it in the family
    • Authors: Ammar Al-Chalabi
      Abstract: Let's start describing ALS on the basis of its cause, not on whether someone obtained a relevant family history, says Ammar Al-Chalabi.
      Citation: Nature
      PubDate: 2017-10-18
      DOI: 10.1038/550S112a
       
  • Fundraising: The Ice Bucket Challenge delivers
    • Authors: Emily Sohn
      Abstract: In 2014, millions of people doused themselves in icy water to raise money for ALS. Was it worth it'
      Citation: Nature
      PubDate: 2017-10-18
      DOI: 10.1038/550S113a
       
  • Machine learning: Calculating disease
    • Authors: Neil Savage
      Abstract: Machine learning might identify patients earlier, predict their outcomes better, and assign them more efficiently to appropriate clinical trials.
      Citation: Nature
      PubDate: 2017-10-18
      DOI: 10.1038/550S115a
       
  • Research round-up
  • Drug therapy: On the treatment trail for ALS
    • Authors: Andrew Scott
      Abstract: The disease remains incurable but there are signs of hope on the horizon.
      Citation: Nature
      PubDate: 2017-10-18
      DOI: 10.1038/550S120a
       
  • Perspective: Untangling the ALS X-Files
    • Authors: Richard Bedlack
      Abstract: Richard Bedlack explains how an open mind led him to some unusual places and unexpected lessons
      Citation: Nature
      PubDate: 2017-10-18
      DOI: 10.1038/550S122a
       
  • The shape of work to come
    • Authors: Emily Anthes
      Pages: 316 - 319
      Abstract: Three ways that the digital revolution is reshaping workforces around the world.
      Citation: Nature 550, 7676 (2017)
      DOI: 10.1038/550316a
      Issue No: Vol. 550, No. 7676
       
 
 
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