Nature (NATURE)

Publications in this journal

• Article: Sema3A regulates bone-mass accrual through sensory innervations.

  Fukuda T, Takeda S, Xu R, Ochi H, Sunamura S, Sato T, Shibata S, Yoshida Y, Gu Z, Kimura A, [......], Xu C, Bando W, Fujita K, Shinomiya K, Hirai T, Asou Y, Enomoto M, Okano H, Okawa A, Itoh H
  Nature 05/2013;
• Article: Heed the father of cladistics

  Quentin Wheeler, Leandro Assis, Olivier Rieppel
  Nature 04/2013; 496:295-296.
• Article: Changes in global nitrogen cycling during the Holocene epoch

  Kendra K. McLauchlan, Joseph J. Williams, Joseph M. Craine, Elizabeth S. Jeffers
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  ABSTRACT: Human activities have doubled the pre-industrial supply of reactive nitrogen on Earth, and future rates of increase are expected to accelerate. Yet little is known about the capacity of the biosphere to buffer increased nitrogen influx. Past changes in global ecosystems following deglaciation at the end of the Pleistocene epoch provide an opportunity to understand better how nitrogen cycling in the terrestrial biosphere responded to changes in carbon cycling. We analysed published records of stable nitrogen isotopic values (δ15N) in sediments from 86 lakes on six continents. Here we show that the value of sedimentary δ15N declined from 15,000 years before present to 7,056 ± 597 years before present, a period of increasing atmospheric carbon dioxide concentrations and terrestrial carbon accumulation. Comparison of the nitrogen isotope record with concomitant carbon accumulation on land and nitrous oxide in the atmosphere suggests millennia of declining nitrogen availability in terrestrial ecosystems during the Pleistocene–Holocene transition around 11,000 years before present. In contrast, we do not observe a consistent change in global sedimentary δ15N values during the past 500 years, despite the potential effects of changing temperature and nitrogen influx from anthropogenic sources. We propose that the lack of a single response may indicate that modern increases in atmospheric carbon dioxide and net carbon sequestration in the biosphere have the potential to offset recent increased supplies of reactive nitrogen in some ecosystems
  Nature 03/2013; 495:352–355.
• Article: CLASP-mediated cortical microtubule organization guides PIN polarization axis.

  Klementina Kakar, Hongtao Zhang, Ben Scheres, Pankaj Dhonukshe
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  ABSTRACT: Recent evidence indicates a correlation between orientation of the plant cortical microtubule cytoskeleton and localization of polar cargoes. However, the molecules and mechanisms that create this correlation have remained unknown. Here we show that, in Arabidopsis thaliana, the microtubule orientation regulators CLASP and MAP65 (refs 3, 4) control the abundance of polarity regulator PINOID kinase at the plasma membrane. By localized upregulation of clathrin-dependent endocytosis at cortical microtubule- and clathrin-rich domains orthogonal to the axis of polarity, PINOID accelerates the removal of auxin transporter PIN proteins from those sites. This mechanism links directional microtubule organization to the polar localization of auxin transporter PIN proteins, and clarifies how microtubule-enriched cell sides are kept distinct from polar delivery domains. Our results identify the molecular machinery that connects microtubule organization to the regulation of the axis of PIN polarization.
  Nature 03/2013; 495(7442):529–533.
• Article: Mutations in prion-like domains in hnRNPA2B1 and hnRNPA1 cause multisystem proteinopathy and ALS.

  Kim HJ, Kim NC, Wang YD, Scarborough EA, Moore J, Diaz Z, Maclea KS, Freibaum B, Li S, Molliex A, [......], Li YR, Ford AF, Gitler AD, Benatar M, King OD, Kimonis VE, Ross ED, Weihl CC, Shorter J, Taylor JP
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  ABSTRACT: Algorithms designed to identify canonical yeast prions predict that around 250 human proteins, including several RNA-binding proteins associated with neurodegenerative disease, harbour a distinctive prion-like domain (PrLD) enriched in uncharged polar amino acids and glycine. PrLDs in RNA-binding proteins are essential for the assembly of ribonucleoprotein granules. However, the interplay between human PrLD function and disease is not understood. Here we define pathogenic mutations in PrLDs of heterogeneous nuclear ribonucleoproteins (hnRNPs) A2B1 and A1 in families with inherited degeneration affecting muscle, brain, motor neuron and bone, and in one case of familial amyotrophic lateral sclerosis. Wild-type hnRNPA2 (the most abundant isoform of hnRNPA2B1) and hnRNPA1 show an intrinsic tendency to assemble into self-seeding fibrils, which is exacerbated by the disease mutations. Indeed, the pathogenic mutations strengthen a 'steric zipper' motif in the PrLD, which accelerates the formation of self-seeding fibrils that cross-seed polymerization of wild-type hnRNP. Notably, the disease mutations promote excess incorporation of hnRNPA2 and hnRNPA1 into stress granules and drive the formation of cytoplasmic inclusions in animal models that recapitulate the human pathology. Thus, dysregulated polymerization caused by a potent mutant steric zipper motif in a PrLD can initiate degenerative disease. Related proteins with PrLDs should therefore be considered candidates for initiating and perhaps propagating proteinopathies of muscle, brain, motor neuron and bone.
  Nature 03/2013;
• Article: CLP1 links tRNA metabolism to progressive motor-neuron loss.

  Toshikatsu Hanada, Stefan Weitzer, Barbara Mair, Christian Bernreuther, Brian J Wainger, Justin Ichida, Reiko Hanada, Michael Orthofer, Shane J Cronin, Vukoslav Komnenovic, [......], Ido Tamir, Johannes Rainer, Reinhard Kofler, Avraham Yaron, Kevin C Eggan, Clifford J Woolf, Markus Glatzel, Ruth Herbst, Javier Martinez, Josef M Penninger
  Nature 03/2013;
• Article: Environmental modification of a genetically based bahaviour pattern in D. melanogaster.

  M A Dow
  Nature 02/2013; 255(5504):172.
• Article: Fast rise times and the physical mechanism of deep earthquakes

  H. Houston, Q. Williams
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  ABSTRACT: A systematic global survey of the rise times and stress drops of deep and intermediate earthquakes is reported. When the rise times are scaled to the seismic moment release of the events, their average is nearly twice as fast for events deeper than about 450 km as for shallower events.
  Nature 02/2013; 352:520.
• Article: Magnetic differentiation of atmospheric dusts

  Oldfield, Hunt, Jones, M.D.H, Chester, Dearing, J.A, Olsson, Prospero, J.M
  Nature 02/2013; 317:516.
• Article: Relictogobius kryzhanovskii and the penetration of Mediterranean gobies into the Black Sea

  Miller P.J
  Nature 02/2013; 208:474-475.
• Article: Co-evolution of a broadly neutralizing HIV-1 antibody and founder virus

  Hua-Xin Liao, Rebecca Lynch, Tongqing Zhou, Feng Gao, S. Munir Alam, Scott D. Boyd, Andrew Z. Fire, Krishna M. Roskin, Chaim A. Schramm, Zhenhai Zhang, [......], Sanjay Srivatsan, Baoshan Zhang, Anqi Zheng, George M. Shaw, Beatrice H. Hahn, Thomas B. Kepler, Bette T. M. Korber, Peter D. Kwong, John R. Mascola, Barton F. Haynes
  Nature 01/2013; advance online publication.
• Article: CALHM1 ion channel mediates purinergic neurotransmission of sweet, bitter and umami tastes

  A. Taruno, V. Vingtdeux, M. Ohmoto, Z. Ma, G. Dvoryanchikov, A. Li, L. Adrien, H. Zhao, S. Leung, M. Abernethy, J. Koppel, P. Davies, M. M. Civan, N. Chaudhari, I. Matsumoto, G. Hellekant, M. G. Tordoff, P. Marambaud, J. K. Foskett
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  ABSTRACT: Recognition of sweet, bitter and umami tastes requires the non-vesicular release from taste bud cells of ATP, which acts as a neurotransmitter to activate afferent neural gustatory pathways. However, how ATP is released to fulfil this function is not fully understood. Here we show that calcium homeostasis modulator 1 (CALHM1), a voltage-gated ion channel, is indispensable for taste-stimuli-evoked ATP release from sweet-, bitter- and umami-sensing taste bud cells. Calhm1 knockout mice have severely impaired perceptions of sweet, bitter and umami compounds, whereas their recognition of sour and salty tastes remains mostly normal. Calhm1 deficiency affects taste perception without interfering with taste cell development or integrity. CALHM1 is expressed specifically in sweet/bitter/umami-sensing type II taste bud cells. Its heterologous expression induces a novel ATP permeability that releases ATP from cells in response to manipulations that activate the CALHM1 ion channel. Knockout of Calhm1 strongly reduces voltage-gated currents in type II cells and taste-evoked ATP release from taste buds without affecting the excitability of taste cells by taste stimuli. Thus, CALHM1 is a voltage-gated ATP-release channel required for sweet, bitter and umami taste perception.
  Nature 01/2013;