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  • 1
    Publication Date: 2014-03-05
    Description: Epithelial folding mediated by apical constriction converts flat epithelial sheets into multilayered, complex tissue structures and is used throughout development in most animals. Little is known, however, about how forces produced near the apical surface of the tissue are transmitted within individual cells to generate the global changes in cell shape that characterize tissue deformation. Here we apply particle tracking velocimetry in gastrulating Drosophila embryos to measure the movement of cytoplasm and plasma membrane during ventral furrow formation. We find that cytoplasmic redistribution during the lengthening phase of ventral furrow formation can be precisely described by viscous flows that quantitatively match the predictions of hydrodynamics. Cell membranes move with the ambient cytoplasm, with little resistance to, or driving force on, the flow. Strikingly, apical constriction produces similar flow patterns in mutant embryos that fail to form cells before gastrulation ('acellular' embryos), such that the global redistribution of cytoplasm mirrors the summed redistribution occurring in individual cells of wild-type embryos. Our results indicate that during the lengthening phase of ventral furrow formation, hydrodynamic behaviour of the cytoplasm provides the predominant mechanism transmitting apically generated forces deep into the tissue and that cell individualization is dispensable.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4111109/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4111109/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉He, Bing -- Doubrovinski, Konstantin -- Polyakov, Oleg -- Wieschaus, Eric -- 5R37HD15587/HD/NICHD NIH HHS/ -- P50 GM 071508/GM/NIGMS NIH HHS/ -- R01 HD015587/HD/NICHD NIH HHS/ -- R37 HD015587/HD/NICHD NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 Apr 17;508(7496):392-6. doi: 10.1038/nature13070. Epub 2014 Mar 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544, USA [2]. ; Department of Physics, Princeton University, Princeton, New Jersey 08544, USA. ; 1] Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544, USA [2] Howard Hughes Medical Institute, Princeton University, Princeton, New Jersey 08544, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24590071" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Membrane/metabolism ; *Cell Polarity ; *Cell Shape ; Cytoplasm/metabolism ; Drosophila melanogaster/*cytology/*embryology ; Female ; Gastrulation ; Hydrodynamics ; Male ; Mesoderm/cytology/metabolism ; *Morphogenesis ; Movement
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  • 2
    Publication Date: 2013-12-18
    Description: Prokaryotic viruses have evolved various mechanisms to transport their genomes across bacterial cell walls. Many bacteriophages use a tail to perform this function, whereas tail-less phages rely on host organelles. However, the tail-less, icosahedral, single-stranded DNA PhiX174-like coliphages do not fall into these well-defined infection processes. For these phages, DNA delivery requires a DNA pilot protein. Here we show that the PhiX174 pilot protein H oligomerizes to form a tube whose function is most probably to deliver the DNA genome across the host's periplasmic space to the cytoplasm. The 2.4 A resolution crystal structure of the in vitro assembled H protein's central domain consists of a 170 A-long alpha-helical barrel. The tube is constructed of ten alpha-helices with their amino termini arrayed in a right-handed super-helical coiled-coil and their carboxy termini arrayed in a left-handed super-helical coiled-coil. Genetic and biochemical studies demonstrate that the tube is essential for infectivity but does not affect in vivo virus assembly. Cryo-electron tomograms show that tubes span the periplasmic space and are present while the genome is being delivered into the host cell's cytoplasm. Both ends of the H protein contain transmembrane domains, which anchor the assembled tubes into the inner and outer cell membranes. The central channel of the H-protein tube is lined with amide and guanidinium side chains. This may be a general property of viral DNA conduits and is likely to be critical for efficient genome translocation into the host.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sun, Lei -- Young, Lindsey N -- Zhang, Xinzheng -- Boudko, Sergei P -- Fokine, Andrei -- Zbornik, Erica -- Roznowski, Aaron P -- Molineux, Ian J -- Rossmann, Michael G -- Fane, Bentley A -- England -- Nature. 2014 Jan 16;505(7483):432-5. doi: 10.1038/nature12816. Epub 2013 Dec 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Biological Sciences, Purdue University, West Lafayette, Indiana 47907, USA [2]. ; 1] School of Plant Sciences and the BIO5 Institute, University of Arizona, Tucson, Arizona 85721, USA [2]. ; 1] Department of Biological Sciences, Purdue University, West Lafayette, Indiana 47907, USA [2] The Research Department, Shriner's Hospital for Children, Portland, Oregon 97239, USA. ; Department of Biological Sciences, Purdue University, West Lafayette, Indiana 47907, USA. ; School of Plant Sciences and the BIO5 Institute, University of Arizona, Tucson, Arizona 85721, USA. ; Molecular Genetics and Microbiology, Institute for Cell and Molecular Biology, The University of Texas at Austin, Austin, Texas 78712, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24336205" target="_blank"〉PubMed〈/a〉
    Keywords: Bacteriophage phi X 174/*chemistry/*metabolism/ultrastructure ; Biological Transport ; Cryoelectron Microscopy ; Crystallography, X-Ray ; Cytoplasm/metabolism/ultrastructure/virology ; DNA, Viral/*metabolism/ultrastructure ; Escherichia coli/cytology/ultrastructure/*virology ; Genome, Viral ; Models, Molecular ; Periplasm/metabolism/ultrastructure ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Viral Proteins/chemistry/metabolism/ultrastructure ; *Virus Assembly
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  • 3
    Publication Date: 2014-11-14
    Description: Films of iron selenide (FeSe) one unit cell thick grown on strontium titanate (SrTiO3 or STO) substrates have recently shown superconducting energy gaps opening at temperatures close to the boiling point of liquid nitrogen (77 kelvin), which is a record for the iron-based superconductors. The gap opening temperature usually sets the superconducting transition temperature Tc, as the gap signals the formation of Cooper pairs, the bound electron states responsible for superconductivity. To understand why Cooper pairs form at such high temperatures, we examine the role of the SrTiO3 substrate. Here we report high-resolution angle-resolved photoemission spectroscopy results that reveal an unexpected characteristic of the single-unit-cell FeSe/SrTiO3 system: shake-off bands suggesting the presence of bosonic modes, most probably oxygen optical phonons in SrTiO3 (refs 5, 6, 7), which couple to the FeSe electrons with only a small momentum transfer. Such interfacial coupling assists superconductivity in most channels, including those mediated by spin fluctuations. Our calculations suggest that this coupling is responsible for raising the superconducting gap opening temperature in single-unit-cell FeSe/SrTiO3.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, J J -- Schmitt, F T -- Moore, R G -- Johnston, S -- Cui, Y-T -- Li, W -- Yi, M -- Liu, Z K -- Hashimoto, M -- Zhang, Y -- Lu, D H -- Devereaux, T P -- Lee, D-H -- Shen, Z-X -- England -- Nature. 2014 Nov 13;515(7526):245-8. doi: 10.1038/nature13894.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Stanford Institute for Materials and Energy Sciences, SLAC National Accelerator Laboratory, Menlo Park, California 94025, USA [2] Departments of Physics and Applied Physics, and Geballe Laboratory for Advanced Materials, Stanford University, Stanford, California 94305, USA. ; Stanford Institute for Materials and Energy Sciences, SLAC National Accelerator Laboratory, Menlo Park, California 94025, USA. ; 1] Department of Physics and Astronomy, University of British Columbia, Vancouver, British Columbia V6T 1Z1, Canada [2] Quantum Matter Institute, University of British Columbia, Vancouver, British Columbia V6T 1Z4, Canada [3] Department of Physics and Astronomy, University of Tennessee, Knoxville, Tennessee 37996-1200, USA. ; Stanford Synchrotron Radiation Lightsource, SLAC National Accelerator Laboratory, Menlo Park, California 94025, USA. ; 1] Stanford Institute for Materials and Energy Sciences, SLAC National Accelerator Laboratory, Menlo Park, California 94025, USA [2] Advanced Light Source, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA. ; 1] Department of Physics, University of California at Berkeley, Berkeley, California 94720, USA [2] Material Science Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25391962" target="_blank"〉PubMed〈/a〉
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  • 4
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    Nature Publishing Group (NPG)
    Publication Date: 2014-07-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moskvitch, Katia -- Susman, Edward -- England -- Nature. 2014 Jul 24;511(7510):391. doi: 10.1038/511391a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25056040" target="_blank"〉PubMed〈/a〉
    Keywords: *Acquired Immunodeficiency Syndrome/drug therapy/epidemiology ; *Aircraft ; Anti-HIV Agents ; Australia ; Congresses as Topic ; *Death ; Developing Countries/statistics & numerical data ; Humans ; Netherlands ; *Research Personnel ; Ukraine
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  • 5
    Publication Date: 2014-09-02
    Description: The abundances of elements in stars are critical clues to stars' origins. Observed star-to-star variations in logarithmic abundance within an open star cluster--a gravitationally bound ensemble of stars in the Galactic plane--are typically only about 0.01 to 0.05 over many elements, which is noticeably smaller than the variation of about 0.06 to 0.3 seen in the interstellar medium from which the stars form. It is unknown why star clusters are so homogenous, and whether homogeneity should also prevail in regions of lower star formation efficiency that do not produce bound clusters. Here we report simulations that trace the mixing of chemical elements as star-forming clouds assemble and collapse. We show that turbulent mixing during cloud assembly naturally produces a stellar abundance scatter at least five times smaller than that in the gas, which is sufficient to explain the observed chemical homogeneity of stars. Moreover, mixing occurs very early, so that regions with star formation efficiencies of about 10 per cent are nearly as well mixed as those with formation efficiencies of about 50 per cent. This implies that even regions that do not form bound clusters are likely to be well mixed, and improves the prospects of using 'chemical tagging' to reconstruct (via their unique chemical signatures, or tags) star clusters whose constituent stars have become unbound from one another and spread across the Galactic disk.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Feng, Yi -- Krumholz, Mark R -- England -- Nature. 2014 Sep 25;513(7519):523-5. doi: 10.1038/nature13662. Epub 2014 Aug 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Astronomy and Astrophysics, University of California, Santa Cruz, California 95064, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25174709" target="_blank"〉PubMed〈/a〉
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  • 6
    Publication Date: 2014-04-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moss, Andrew -- Jensen, Eric -- Gusset, Markus -- England -- Nature. 2014 Apr 10;508(7495):186. doi: 10.1038/508186d.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Chester Zoo, UK. ; University of Warwick, Coventry, UK. ; World Association of Zoos and Aquariums, Gland, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24717506" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Animals, Zoo ; *Biodiversity ; Conservation of Natural Resources/*trends ; Ecology/*education
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  • 7
    Publication Date: 2014-11-11
    Description: Autophagy is an evolutionarily conserved catabolic process that recycles nutrients upon starvation and maintains cellular energy homeostasis. Its acute regulation by nutrient-sensing signalling pathways is well described, but its longer-term transcriptional regulation is not. The nuclear receptors peroxisome proliferator-activated receptor-alpha (PPARalpha) and farnesoid X receptor (FXR) are activated in the fasted and fed liver, respectively. Here we show that both PPARalpha and FXR regulate hepatic autophagy in mice. Pharmacological activation of PPARalpha reverses the normal suppression of autophagy in the fed state, inducing autophagic lipid degradation, or lipophagy. This response is lost in PPARalpha knockout (Ppara(-/-), also known as Nr1c1(-/-)) mice, which are partially defective in the induction of autophagy by fasting. Pharmacological activation of the bile acid receptor FXR strongly suppresses the induction of autophagy in the fasting state, and this response is absent in FXR knockout (Fxr(-/-), also known as Nr1h4(-/-)) mice, which show a partial defect in suppression of hepatic autophagy in the fed state. PPARalpha and FXR compete for binding to shared sites in autophagic gene promoters, with opposite transcriptional outputs. These results reveal complementary, interlocking mechanisms for regulation of autophagy by nutrient status.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4267857/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4267857/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Jae Man -- Wagner, Martin -- Xiao, Rui -- Kim, Kang Ho -- Feng, Dan -- Lazar, Mitchell A -- Moore, David D -- DK43806/DK/NIDDK NIH HHS/ -- P30 DK019525/DK/NIDDK NIH HHS/ -- P30DX56338-05A2/PHS HHS/ -- P39CA125123-04/CA/NCI NIH HHS/ -- R01 DK049780/DK/NIDDK NIH HHS/ -- R01 DK49780/DK/NIDDK NIH HHS/ -- R37 DK043806/DK/NIDDK NIH HHS/ -- S10RR027783-01A1/RR/NCRR NIH HHS/ -- U54HD-07495-39/HD/NICHD NIH HHS/ -- England -- Nature. 2014 Dec 4;516(7529):112-5. doi: 10.1038/nature13961. Epub 2014 Nov 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas 77030, USA. ; Division of Endocrinology, Diabetes, and Metabolism and the Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19014, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25383539" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autophagy/genetics/*physiology ; Cell Line ; Cells, Cultured ; Fasting/physiology ; Gene Expression Regulation ; Hepatocytes/metabolism ; Liver/cytology/*metabolism/ultrastructure ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Microtubule-Associated Proteins/genetics/metabolism ; PPAR alpha ; Receptors, Cytoplasmic and Nuclear/genetics/*metabolism
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  • 8
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    Nature Publishing Group (NPG)
    Publication Date: 2014-07-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alperin, Juan Pablo -- England -- Nature. 2014 Jul 10;511(7508):155. doi: 10.1038/511155c.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stanford University, California, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25008513" target="_blank"〉PubMed〈/a〉
    Keywords: *Science
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  • 9
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    Nature Publishing Group (NPG)
    Publication Date: 2014-10-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abbott, Alison -- Callaway, Ewen -- England -- Nature. 2014 Oct 9;514(7521):153. doi: 10.1038/514153a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25297415" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Entorhinal Cortex/*cytology/physiology ; Hippocampus/*cytology/physiology ; Humans ; Models, Neurological ; *Nobel Prize ; Space Perception/*physiology
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  • 10
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    Nature Publishing Group (NPG)
    Publication Date: 2014-11-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ledford, Heidi -- England -- Nature. 2014 Nov 13;515(7526):182-4. doi: 10.1038/515182a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25391943" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antidepressive Agents/pharmacology/therapeutic use ; Biomedical Research/economics/*statistics & numerical data/*trends ; Depression/*epidemiology/genetics/psychology/*therapy ; Depressive Disorder/epidemiology/genetics/psychology/therapy ; Disease Models, Animal ; Humans ; Mice ; *Neoplasms ; Neurosciences/*trends ; Stress, Psychological/epidemiology/etiology/therapy
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  • 11
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    Nature Publishing Group (NPG)
    Publication Date: 2014-06-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Enriquez, Jose Rafael Martinez -- England -- Nature. 2014 Jun 5;510(7503):35. doi: 10.1038/510035d.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Autonomous University of Mexico, Mexico City, Mexico.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24899294" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Drama/*history ; Literature, Modern/*history ; Science/*history ; Technology/*history
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  • 12
    Publication Date: 2014-09-19
    Description: Characterization studies now have a dominant role in the field of exoplanets. Such studies include the measurement of an exoplanet's bulk density, its brightness temperature and the chemical composition of its atmosphere. The use of space telescopes has played a key part in the characterization of transiting exoplanets. These facilities offer astronomers data of exquisite precision and temporal sampling as well as access to wavelength regions of the electromagnetic spectrum that are inaccessible from the ground. Space missions such as the Hubble Space Telescope, Microvariability and Oscillations of Stars (MOST), Spitzer Space Telescope, Convection, Rotation and Planetary Transits (CoRoT), and Kepler have rapidly advanced our knowledge of the physical properties of exoplanets and have blazed a trail for a series of future space missions that will help us to understand the observed diversity of exoplanets.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hatzes, Artie P -- England -- Nature. 2014 Sep 18;513(7518):353-7. doi: 10.1038/nature13783.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Thuringer Landessternwarte Tautenburg, Sternwarte 5, D-07778, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25230657" target="_blank"〉PubMed〈/a〉
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  • 13
    Publication Date: 2014-03-29
    Description: Subduction zones become congested when they try to consume buoyant, exotic crust. The accretionary mountain belts (orogens) that form at these convergent plate margins have been the principal sites of lateral continental growth through Earth's history. Modern examples of accretionary margins are the North American Cordilleras and southwest Pacific subduction zones. The geologic record contains abundant accretionary orogens, such as the Tasmanides, along the eastern margin of the supercontinent Gondwana, and the Altaides, which formed on the southern margin of Laurasia. In modern and ancient examples of long-lived accretionary orogens, the overriding plate is subjected to episodes of crustal extension and back-arc basin development, often related to subduction rollback and transient episodes of orogenesis and crustal shortening, coincident with accretion of exotic crust. Here we present three-dimensional dynamic models that show how accretionary margins evolve from the initial collision, through a period of plate margin instability, to re-establishment of a stable convergent margin. The models illustrate how significant curvature of the orogenic system develops, as well as the mechanism for tectonic escape of the back-arc region. The complexity of the morphology and the evolution of the system are caused by lateral rollback of a tightly arcuate trench migrating parallel to the plate boundary and orthogonally to the convergence direction. We find geological and geophysical evidence for this process in the Tasmanides of eastern Australia, and infer that this is a recurrent and global phenomenon.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moresi, L -- Betts, P G -- Miller, M S -- Cayley, R A -- England -- Nature. 2014 Apr 10;508(7495):245-8. doi: 10.1038/nature13033. Epub 2014 Mar 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] School of Geosciences, Monash University, Clayton, Victoria 3800, Australia [2] School of Mathematical Sciences, Monash University, Clayton, Victoria 3800, Australia [3] School of Earth Sciences, University of Melbourne, Parkville, Victoria 3010, Australia. ; School of Geosciences, Monash University, Clayton, Victoria 3800, Australia. ; Department of Earth Sciences, University of Southern California, Los Angeles, California 90089, USA. ; Geological Survey of Victoria, Melbourne, Victoria 3001, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24670638" target="_blank"〉PubMed〈/a〉
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  • 14
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    Nature Publishing Group (NPG)
    Publication Date: 2014-02-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reardon, Sara -- England -- Nature. 2014 Feb 20;506(7488):284-6. doi: 10.1038/506284a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24553224" target="_blank"〉PubMed〈/a〉
    Keywords: Capital Punishment/*legislation & jurisprudence ; Criminals/*legislation & jurisprudence/*psychology ; Florida ; Humans ; Intellectual Disability/*diagnosis/*psychology ; *Intelligence Tests ; Male
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  • 15
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    Nature Publishing Group (NPG)
    Publication Date: 2014-11-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abbott, Alison -- Nosengo, Nicola -- England -- Nature. 2014 Nov 13;515(7526):171. doi: 10.1038/515171a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25391936" target="_blank"〉PubMed〈/a〉
    Keywords: Disaster Planning/legislation & jurisprudence ; Disasters/prevention & control ; Earthquakes/*mortality ; Homicide/*legislation & jurisprudence ; Humans ; Italy ; Malpractice/*legislation & jurisprudence ; Research Personnel/*legislation & jurisprudence
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  • 16
    Publication Date: 2014-11-21
    Description: The basic body plan and major physiological axes have been highly conserved during mammalian evolution, yet only a small fraction of the human genome sequence appears to be subject to evolutionary constraint. To quantify cis- versus trans-acting contributions to mammalian regulatory evolution, we performed genomic DNase I footprinting of the mouse genome across 25 cell and tissue types, collectively defining approximately 8.6 million transcription factor (TF) occupancy sites at nucleotide resolution. Here we show that mouse TF footprints conjointly encode a regulatory lexicon that is approximately 95% similar with that derived from human TF footprints. However, only approximately 20% of mouse TF footprints have human orthologues. Despite substantial turnover of the cis-regulatory landscape, nearly half of all pairwise regulatory interactions connecting mouse TF genes have been maintained in orthologous human cell types through evolutionary innovation of TF recognition sequences. Furthermore, the higher-level organization of mouse TF-to-TF connections into cellular network architectures is nearly identical with human. Our results indicate that evolutionary selection on mammalian gene regulation is targeted chiefly at the level of trans-regulatory circuitry, enabling and potentiating cis-regulatory plasticity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4405208/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4405208/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stergachis, Andrew B -- Neph, Shane -- Sandstrom, Richard -- Haugen, Eric -- Reynolds, Alex P -- Zhang, Miaohua -- Byron, Rachel -- Canfield, Theresa -- Stelhing-Sun, Sandra -- Lee, Kristen -- Thurman, Robert E -- Vong, Shinny -- Bates, Daniel -- Neri, Fidencio -- Diegel, Morgan -- Giste, Erika -- Dunn, Douglas -- Vierstra, Jeff -- Hansen, R Scott -- Johnson, Audra K -- Sabo, Peter J -- Wilken, Matthew S -- Reh, Thomas A -- Treuting, Piper M -- Kaul, Rajinder -- Groudine, Mark -- Bender, M A -- Borenstein, Elhanan -- Stamatoyannopoulos, John A -- FDK095678A/PHS HHS/ -- R01 EY021482/EY/NEI NIH HHS/ -- R37 DK044746/DK/NIDDK NIH HHS/ -- R37DK44746/DK/NIDDK NIH HHS/ -- RC2 HG005654/HG/NHGRI NIH HHS/ -- RC2HG005654/HG/NHGRI NIH HHS/ -- T32 GM007266/GM/NIGMS NIH HHS/ -- U01ES01156/ES/NIEHS NIH HHS/ -- U54 HG007010/HG/NHGRI NIH HHS/ -- U54HG004592/HG/NHGRI NIH HHS/ -- U54HG007010/HG/NHGRI NIH HHS/ -- England -- Nature. 2014 Nov 20;515(7527):365-70. doi: 10.1038/nature13972.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genome Sciences, University of Washington, Seattle, Washington 98195, USA. ; Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA. ; 1] Department of Genome Sciences, University of Washington, Seattle, Washington 98195, USA [2] Department of Medicine, University of Washington, Seattle, Washington 98195, USA. ; Department of Biological Structure, University of Washington, Seattle, Washington 98195, USA. ; Department of Comparative Medicine, University of Washington, Seattle, Washington 98195, USA. ; 1] Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA [2] Division of Radiation Oncology, University of Washington, Seattle, Washington 98195, USA. ; 1] Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA [2] Department of Pediatrics, University of Washington, Seattle, Washington 98195, USA. ; 1] Department of Genome Sciences, University of Washington, Seattle, Washington 98195, USA [2] Department of Computer Science and Engineering, University of Washington, Seattle, Washington 98102, USA [3] Santa Fe Institute, Santa Fe, New Mexico 87501, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25409825" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Conserved Sequence/*genetics ; DNA Footprinting ; *Evolution, Molecular ; Gene Expression Regulation, Developmental/genetics ; Gene Regulatory Networks/genetics ; Humans ; Mammals/*genetics ; Mice ; Regulatory Sequences, Nucleic Acid/*genetics ; Transcription Factors/*genetics/*metabolism
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  • 17
    Publication Date: 2014-08-01
    Description: The translational control of oncoprotein expression is implicated in many cancers. Here we report an eIF4A RNA helicase-dependent mechanism of translational control that contributes to oncogenesis and underlies the anticancer effects of silvestrol and related compounds. For example, eIF4A promotes T-cell acute lymphoblastic leukaemia development in vivo and is required for leukaemia maintenance. Accordingly, inhibition of eIF4A with silvestrol has powerful therapeutic effects against murine and human leukaemic cells in vitro and in vivo. We use transcriptome-scale ribosome footprinting to identify the hallmarks of eIF4A-dependent transcripts. These include 5' untranslated region (UTR) sequences such as the 12-nucleotide guanine quartet (CGG)4 motif that can form RNA G-quadruplex structures. Notably, among the most eIF4A-dependent and silvestrol-sensitive transcripts are a number of oncogenes, superenhancer-associated transcription factors, and epigenetic regulators. Hence, the 5' UTRs of select cancer genes harbour a targetable requirement for the eIF4A RNA helicase.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4492470/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4492470/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wolfe, Andrew L -- Singh, Kamini -- Zhong, Yi -- Drewe, Philipp -- Rajasekhar, Vinagolu K -- Sanghvi, Viraj R -- Mavrakis, Konstantinos J -- Jiang, Man -- Roderick, Justine E -- Van der Meulen, Joni -- Schatz, Jonathan H -- Rodrigo, Christina M -- Zhao, Chunying -- Rondou, Pieter -- de Stanchina, Elisa -- Teruya-Feldstein, Julie -- Kelliher, Michelle A -- Speleman, Frank -- Porco, John A Jr -- Pelletier, Jerry -- Ratsch, Gunnar -- Wendel, Hans-Guido -- GM-067041/GM/NIGMS NIH HHS/ -- GM-073855/GM/NIGMS NIH HHS/ -- MOP-10653/Canadian Institutes of Health Research/Canada -- P30 CA008748/CA/NCI NIH HHS/ -- R01 CA142798/CA/NCI NIH HHS/ -- R01-CA142798-01/CA/NCI NIH HHS/ -- England -- Nature. 2014 Sep 4;513(7516):65-70. doi: 10.1038/nature13485. Epub 2014 Jul 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Cancer Biology and Genetics, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA [2] Weill Cornell Graduate School of Medical Sciences, New York, New York 10065, USA [3]. ; 1] Cancer Biology and Genetics, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA [2]. ; Computational Biology Department, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA. ; Stem Cell Center and Developmental Biology Program, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA. ; Cancer Biology and Genetics, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA. ; 1] Cancer Biology and Genetics, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA [2] Novartis, Cambridge, Massachusetts 02139, USA (K.J.M.); The University of Arizona Cancer Center, Tucson, Arizona 85719, USA (J.H.S.). ; Department of Cancer Biology, University of Massachusetts Medical School, Worcester, Massachusetts 01605 USA. ; 1] Cancer Biology and Genetics, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA [2] Center for Medical Genetics, Ghent University Hospital, De Pintelaan 185, B-9000 Ghent, Belgium. ; 1] Cancer Biology and Genetics, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA [2] Department of Medicine, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA [3] Novartis, Cambridge, Massachusetts 02139, USA (K.J.M.); The University of Arizona Cancer Center, Tucson, Arizona 85719, USA (J.H.S.). ; Department of Chemistry, Center for Chemical Methodology and Library Development, Boston University, Boston, Massachusetts 02215, USA. ; Center for Medical Genetics, Ghent University Hospital, De Pintelaan 185, B-9000 Ghent, Belgium. ; Molecular Pharmacology Program, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA. ; Department of Pathology, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA. ; 1] Department of Biochemistry, McGill University, Montreal, Quebec H3G 1Y6, Canada [2] Department of Oncology, McGill University, Montreal, Quebec H3G 1Y6, Canada [3] The Rosalind and Morris Goodman Cancer Research Center, McGill University, Montreal, Quebec H3G 1Y6, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25079319" target="_blank"〉PubMed〈/a〉
    Keywords: 5' Untranslated Regions/*genetics ; Animals ; Antineoplastic Agents, Phytogenic/pharmacology/therapeutic use ; Base Sequence ; Cell Line, Tumor ; Epigenesis, Genetic ; Eukaryotic Initiation Factor-4A/*metabolism ; Female ; *G-Quadruplexes ; Humans ; Mice ; Mice, Inbred C57BL ; Nucleotide Motifs ; Oncogene Proteins/*biosynthesis/*genetics ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/drug ; therapy/genetics/*metabolism ; *Protein Biosynthesis/drug effects ; Ribosomes/metabolism ; Transcription Factors/metabolism ; Transcription, Genetic/drug effects/genetics ; Triterpenes/pharmacology
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  • 18
    Publication Date: 2013-11-22
    Description: Human body-surface epithelia coexist in close association with complex bacterial communities and are protected by a variety of antibacterial proteins. C-type lectins of the RegIII family are bactericidal proteins that limit direct contact between bacteria and the intestinal epithelium and thus promote tolerance to the intestinal microbiota. RegIII lectins recognize their bacterial targets by binding peptidoglycan carbohydrate, but the mechanism by which they kill bacteria is unknown. Here we elucidate the mechanistic basis for RegIII bactericidal activity. We show that human RegIIIalpha (also known as HIP/PAP) binds membrane phospholipids and kills bacteria by forming a hexameric membrane-permeabilizing oligomeric pore. We derive a three-dimensional model of the RegIIIalpha pore by docking the RegIIIalpha crystal structure into a cryo-electron microscopic map of the pore complex, and show that the model accords with experimentally determined properties of the pore. Lipopolysaccharide inhibits RegIIIalpha pore-forming activity, explaining why RegIIIalpha is bactericidal for Gram-positive but not Gram-negative bacteria. Our findings identify C-type lectins as mediators of membrane attack in the mucosal immune system, and provide detailed insight into an antibacterial mechanism that promotes mutualism with the resident microbiota.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4160023/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4160023/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mukherjee, Sohini -- Zheng, Hui -- Derebe, Mehabaw G -- Callenberg, Keith M -- Partch, Carrie L -- Rollins, Darcy -- Propheter, Daniel C -- Rizo, Josep -- Grabe, Michael -- Jiang, Qiu-Xing -- Hooper, Lora V -- C06 RR30414/RR/NCRR NIH HHS/ -- F32 DK100074/DK/NIDDK NIH HHS/ -- GM093271/GM/NIGMS NIH HHS/ -- R01 DK070855/DK/NIDDK NIH HHS/ -- R01 NS040944/NS/NINDS NIH HHS/ -- R01 NS40944/NS/NINDS NIH HHS/ -- R01GM088745/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 Jan 2;505(7481):103-7. doi: 10.1038/nature12729. Epub 2013 Nov 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. ; Department of Cell Biology, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. ; Department of Biological Sciences, University of Pittsburgh, and Joint Carnegie Mellon University-University of Pittsburgh PhD Program in Computational Biology, Pittsburgh, Pennsylvania 15261, USA. ; Department of Chemistry and Biochemistry, University of California, Santa Cruz, California 95064, USA. ; Department of Biochemistry and Department of Pharmacology, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. ; 1] Department of Biological Sciences, University of Pittsburgh, and Joint Carnegie Mellon University-University of Pittsburgh PhD Program in Computational Biology, Pittsburgh, Pennsylvania 15261, USA [2] Cardiovascular Research Institute, University of California, San Francisco, San Francisco, California 94143, USA. ; 1] Department of Cell Biology, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA [2]. ; 1] Department of Immunology, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA [2] The Howard Hughes Medical Institute, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA [3].〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24256734" target="_blank"〉PubMed〈/a〉
    Keywords: Anti-Bacterial Agents/chemistry/immunology/*metabolism/pharmacology ; Antigens, Neoplasm/chemistry/immunology/*metabolism ; Biomarkers, Tumor/antagonists & inhibitors/chemistry/immunology/*metabolism ; Cell Membrane Permeability/drug effects ; Cryoelectron Microscopy ; Crystallography, X-Ray ; Gram-Negative Bacteria/drug effects/immunology/metabolism ; Humans ; Immunity, Mucosal/drug effects/immunology ; Intestines/*chemistry/immunology/microbiology ; Lectins, C-Type/antagonists & inhibitors/chemistry/immunology/*metabolism ; Lipopolysaccharides/pharmacology ; Listeria monocytogenes/drug effects/immunology/metabolism ; Microbial Viability/drug effects ; Models, Molecular ; Peptidoglycan/metabolism ; Phospholipids/metabolism ; Porins/antagonists & inhibitors/chemistry/*metabolism ; Symbiosis
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  • 19
    Publication Date: 2014-07-22
    Description: Massive outflows driven by active galactic nuclei are widely recognized to have a key role in the evolution of galaxies, by heating the ambient gas, expelling it from the nuclear regions, and thereby affecting the star-formation histories of the galaxy bulges. It has been proposed that the powerful jets of relativistic particles (such as electrons) launched by some active nuclei can both accelerate and heat the molecular gas, which often dominates the mass budgets of the outflows. Clear evidence for this mechanism, in the form of detailed associations between the molecular gas kinematics and features in the radio-emitting jets, has however been lacking. Here we report that the warm molecular hydrogen gas in the western radio lobe of the Seyfert galaxy IC 5063 is moving at high velocities-up to about 600 kilometres per second-relative to the galaxy disk. This suggests that the molecules have been accelerated by fast shocks driven into the interstellar medium by the expanding radio jets. These results demonstrate the general feasibility of accelerating molecular outflows in fast shocks driven by active nuclei.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tadhunter, C -- Morganti, R -- Rose, M -- Oonk, J B R -- Oosterloo, T -- England -- Nature. 2014 Jul 24;511(7510):440-3. doi: 10.1038/nature13520. Epub 2014 Jul 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physics and Astronomy, University of Sheffield, Sheffield S3 7RH, UK. ; 1] ASTRON, The Netherlands Institute of Radio Astronomy, PO Box 2, 7990 AA, Dwingeloo, The Netherlands [2] Kapteyn Astronomical Institute, University of Groningen, PO Box 800, 9700 AV Groningen, The Netherlands. ; Harvard-Smithsonian Center for Astrophysics, 60 Garden Street, Cambridge, Massachusetts 02138, USA. ; ASTRON, The Netherlands Institute of Radio Astronomy, PO Box 2, 7990 AA, Dwingeloo, The Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25043049" target="_blank"〉PubMed〈/a〉
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  • 20
    Publication Date: 2014-08-01
    Description: The CRISPR-associated protein Cas9 is an RNA-guided endonuclease that cleaves double-stranded DNA bearing sequences complementary to a 20-nucleotide segment in the guide RNA. Cas9 has emerged as a versatile molecular tool for genome editing and gene expression control. RNA-guided DNA recognition and cleavage strictly require the presence of a protospacer adjacent motif (PAM) in the target DNA. Here we report a crystal structure of Streptococcus pyogenes Cas9 in complex with a single-molecule guide RNA and a target DNA containing a canonical 5'-NGG-3' PAM. The structure reveals that the PAM motif resides in a base-paired DNA duplex. The non-complementary strand GG dinucleotide is read out via major-groove interactions with conserved arginine residues from the carboxy-terminal domain of Cas9. Interactions with the minor groove of the PAM duplex and the phosphodiester group at the +1 position in the target DNA strand contribute to local strand separation immediately upstream of the PAM. These observations suggest a mechanism for PAM-dependent target DNA melting and RNA-DNA hybrid formation. Furthermore, this study establishes a framework for the rational engineering of Cas9 enzymes with novel PAM specificities.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4176945/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4176945/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anders, Carolin -- Niewoehner, Ole -- Duerst, Alessia -- Jinek, Martin -- 337284/European Research Council/International -- England -- Nature. 2014 Sep 25;513(7519):569-73. doi: 10.1038/nature13579. Epub 2014 Jul 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Zurich, Winterthurerstrasse 190, CH-8057 Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25079318" target="_blank"〉PubMed〈/a〉
    Keywords: Arginine/genetics/metabolism ; *Base Pairing ; Base Sequence ; CRISPR-Associated Proteins/*metabolism ; Crystallography, X-Ray ; DNA/*chemistry/genetics/*metabolism ; Endonucleases/*metabolism ; Models, Molecular ; Nucleic Acid Denaturation ; *Nucleotide Motifs ; Protein Conformation ; RNA, Guide/chemistry/genetics/metabolism ; Streptococcus pyogenes/*enzymology ; Substrate Specificity
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  • 21
    Publication Date: 2014-09-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Muller, Franz-Josef -- Loring, Jeanne F -- England -- Nature. 2014 Sep 25;513(7519):498-9. doi: 10.1038/513498a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Zentrum fur Integrative Psychiatrie Kiel, Universitatsklinikum Schleswig-Holstein, 24105 Kiel, Germany. ; Department of Chemical Physiology, Center for Regenerative Medicine, The Scripps Research Institute, California 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25254472" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Cell Differentiation/*genetics ; *Cell Engineering/methods ; Cellular Reprogramming/genetics ; Epigenesis, Genetic ; Gene Expression Profiling/methods ; Gene Regulatory Networks/*genetics ; Humans ; Induced Pluripotent Stem Cells/cytology/metabolism ; Models, Biological ; Regenerative Medicine ; Social Networking ; *Software ; Stem Cells/*cytology/*metabolism
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  • 22
    Publication Date: 2014-02-18
    Description: The rapid turnover of the mammalian intestinal epithelium is supported by stem cells located around the base of the crypt. In addition to the Lgr5 marker, intestinal stem cells have been associated with other markers that are expressed heterogeneously within the crypt base region. Previous quantitative clonal fate analyses have led to the proposal that homeostasis occurs as the consequence of neutral competition between dividing stem cells. However, the short-term behaviour of individual Lgr5(+) cells positioned at different locations within the crypt base compartment has not been resolved. Here we establish the short-term dynamics of intestinal stem cells using the novel approach of continuous intravital imaging of Lgr5- Confetti mice. We find that Lgr5(+) cells in the upper part of the niche (termed 'border cells') can be passively displaced into the transit-amplifying domain, after the division of proximate cells, implying that the determination of stem-cell fate can be uncoupled from division. Through quantitative analysis of individual clonal lineages, we show that stem cells at the crypt base, termed 'central cells', experience a survival advantage over border stem cells. However, through the transfer of stem cells between the border and central regions, all Lgr5(+) cells are endowed with long-term self-renewal potential. These findings establish a novel paradigm for stem-cell maintenance in which a dynamically heterogeneous cell population is able to function long term as a single stem-cell pool.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3964820/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3964820/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ritsma, Laila -- Ellenbroek, Saskia I J -- Zomer, Anoek -- Snippert, Hugo J -- de Sauvage, Frederic J -- Simons, Benjamin D -- Clevers, Hans -- van Rheenen, Jacco -- 092096/Wellcome Trust/United Kingdom -- 098357/Wellcome Trust/United Kingdom -- 098357/Z/12/Z/Wellcome Trust/United Kingdom -- England -- Nature. 2014 Mar 20;507(7492):362-5. doi: 10.1038/nature12972. Epub 2014 Feb 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Cancer Genomics Netherlands, Hubrecht Institute-KNAW and University Medical Centre Utrecht, Uppsalalaan 8, 3584 CT Utrecht, The Netherlands [2]. ; Cancer Genomics Netherlands, Hubrecht Institute-KNAW and University Medical Centre Utrecht, Uppsalalaan 8, 3584 CT Utrecht, The Netherlands. ; University Medical Centre Utrecht, Universiteitsweg 100, 3584 CG Utrecht, The Netherlands. ; Department of Molecular Biology, Genentech Inc., 1 DNA Way, South San Francisco, California 94080, USA. ; 1] Cavendish Laboratory, Department of Physics, J. J. Thomson Avenue, University of Cambridge, Cambridge CB3 0HE, UK [2] The Wellcome Trust/Cancer Research UK Gurdon Institute, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK [3] The Wellcome Trust/Medical Research Council Stem Cell Institute, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24531760" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division ; Cell Lineage ; Cell Survival ; Clone Cells/cytology ; Female ; *Homeostasis ; Intestinal Mucosa/*cytology ; Male ; Mice ; Models, Biological ; Molecular Imaging ; Receptors, G-Protein-Coupled/genetics/metabolism ; *Single-Cell Analysis ; Stem Cells/*cytology
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  • 23
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    Nature Publishing Group (NPG)
    Publication Date: 2014-02-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levermann, Anders -- England -- Nature. 2014 Feb 6;506(7486):27-9. doi: 10.1038/506027a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Potsdam Institute for Climate Impact Research, Germany; and is at the Institute of Physics, Potsdam University, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24499903" target="_blank"〉PubMed〈/a〉
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  • 24
    Publication Date: 2014-12-19
    Description: The technological appeal of multiferroics is the ability to control magnetism with electric field. For devices to be useful, such control must be achieved at room temperature. The only single-phase multiferroic material exhibiting unambiguous magnetoelectric coupling at room temperature is BiFeO3 (refs 4 and 5). Its weak ferromagnetism arises from the canting of the antiferromagnetically aligned spins by the Dzyaloshinskii-Moriya (DM) interaction. Prior theory considered the symmetry of the thermodynamic ground state and concluded that direct 180-degree switching of the DM vector by the ferroelectric polarization was forbidden. Instead, we examined the kinetics of the switching process, something not considered previously in theoretical work. Here we show a deterministic reversal of the DM vector and canted moment using an electric field at room temperature. First-principles calculations reveal that the switching kinetics favours a two-step switching process. In each step the DM vector and polarization are coupled and 180-degree deterministic switching of magnetization hence becomes possible, in agreement with experimental observation. We exploit this switching to demonstrate energy-efficient control of a spin-valve device at room temperature. The energy per unit area required is approximately an order of magnitude less than that needed for spin-transfer torque switching. Given that the DM interaction is fundamental to single-phase multiferroics and magnetoelectrics, our results suggest ways to engineer magnetoelectric switching and tailor technologically pertinent functionality for nanometre-scale, low-energy-consumption, non-volatile magnetoelectronics.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heron, J T -- Bosse, J L -- He, Q -- Gao, Y -- Trassin, M -- Ye, L -- Clarkson, J D -- Wang, C -- Liu, Jian -- Salahuddin, S -- Ralph, D C -- Schlom, D G -- Iniguez, J -- Huey, B D -- Ramesh, R -- England -- Nature. 2014 Dec 18;516(7531):370-3. doi: 10.1038/nature14004.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Materials Science and Engineering, Cornell University, Ithaca, New York 14853, USA. ; Department of Materials Science and Engineering, University of Connecticut, Storrs, Connecticut 06269, USA. ; Department of Physics, Durham University, Durham DH1 3LE, UK. ; 1] Department of Physics, University of California, Berkeley, California 94720, USA [2] School of Materials Science and Engineering, and State Key Lab of New Ceramics and Fine Processing, Tsinghua University, Beijing 100084, China. ; Department of Materials, ETH Zurich, Vladimir-Prelog-Weg 4 10, 8093 Zurich, Switzerland. ; Department of Materials Science and Engineering, University of California, Berkeley, California 94720, USA. ; Department of Physics, Cornell University, Ithaca, New York 14853, USA. ; Department of Physics, University of California, Berkeley, California 94720, USA. ; Department of Electrical Engineering and Computer Science, University of California, Berkeley, California 94720, USA. ; 1] Department of Physics, Cornell University, Ithaca, New York 14853, USA [2] Kavli Institute at Cornell for Nanoscale Science, Ithaca, New York 14853, USA. ; 1] Department of Materials Science and Engineering, Cornell University, Ithaca, New York 14853, USA [2] Kavli Institute at Cornell for Nanoscale Science, Ithaca, New York 14853, USA. ; Institut de Ciencia de Materials de Barcelona (ICMAB-CSIC), Campus UAB, 08193 Bellaterra, Spain. ; 1] Department of Materials Science and Engineering, University of Connecticut, Storrs, Connecticut 06269, USA [2] Institute of Materials Science, University of Connecticut, Storrs, Connecticut 06269, USA. ; 1] Department of Physics, University of California, Berkeley, California 94720, USA [2] Department of Materials Science and Engineering, University of California, Berkeley, California 94720, USA [3] Materials Science Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25519134" target="_blank"〉PubMed〈/a〉
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  • 25
    Publication Date: 2014-04-30
    Description: Sensory proteins must relay structural signals from the sensory site over large distances to regulatory output domains. Phytochromes are a major family of red-light-sensing kinases that control diverse cellular functions in plants, bacteria and fungi. Bacterial phytochromes consist of a photosensory core and a carboxy-terminal regulatory domain. Structures of photosensory cores are reported in the resting state and conformational responses to light activation have been proposed in the vicinity of the chromophore. However, the structure of the signalling state and the mechanism of downstream signal relay through the photosensory core remain elusive. Here we report crystal and solution structures of the resting and activated states of the photosensory core of the bacteriophytochrome from Deinococcus radiodurans. The structures show an open and closed form of the dimeric protein for the activated and resting states, respectively. This nanometre-scale rearrangement is controlled by refolding of an evolutionarily conserved 'tongue', which is in contact with the chromophore. The findings reveal an unusual mechanism in which atomic-scale conformational changes around the chromophore are first amplified into an angstrom-scale distance change in the tongue, and further grow into a nanometre-scale conformational signal. The structural mechanism is a blueprint for understanding how phytochromes connect to the cellular signalling network.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4015848/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4015848/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takala, Heikki -- Bjorling, Alexander -- Berntsson, Oskar -- Lehtivuori, Heli -- Niebling, Stephan -- Hoernke, Maria -- Kosheleva, Irina -- Henning, Robert -- Menzel, Andreas -- Ihalainen, Janne A -- Westenhoff, Sebastian -- 1R24GM111072/GM/NIGMS NIH HHS/ -- 279944/European Research Council/International -- R24 GM111072/GM/NIGMS NIH HHS/ -- England -- Nature. 2014 May 8;509(7499):245-8. doi: 10.1038/nature13310. Epub 2014 Apr 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Nanoscience Center, Department of Biological and Environmental Science, University of Jyvaskyla, 40014 Jyvaskyla, Finland [2] Department of Chemistry and Molecular Biology, University of Gothenburg, 40530 Gothenburg, Sweden [3]. ; 1] Department of Chemistry and Molecular Biology, University of Gothenburg, 40530 Gothenburg, Sweden [2]. ; Department of Chemistry and Molecular Biology, University of Gothenburg, 40530 Gothenburg, Sweden. ; Nanoscience Center, Department of Biological and Environmental Science, University of Jyvaskyla, 40014 Jyvaskyla, Finland. ; Center for Advanced Radiation Sources, The University of Chicago, Illinois 60637, USA. ; Paul Scherrer Institut, 5232 Villigen PSI, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24776794" target="_blank"〉PubMed〈/a〉
    Keywords: Bacterial Proteins/*chemistry/*metabolism/radiation effects ; Binding Sites ; Crystallography, X-Ray ; Deinococcus/*chemistry ; *Light Signal Transduction/radiation effects ; Models, Molecular ; Phytochrome/chemistry/metabolism/radiation effects ; Protein Conformation/radiation effects
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  • 26
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    Nature Publishing Group (NPG)
    Publication Date: 2014-02-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levy, Andre -- England -- Nature. 2014 Feb 13;506(7487):159. doi: 10.1038/506159d.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉ISPA, Lisbon, Portugal.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24522592" target="_blank"〉PubMed〈/a〉
    Keywords: Fellowships and Scholarships/economics ; Financing, Government/*economics ; Portugal ; Research/*economics/trends ; Research Support as Topic/*economics
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  • 27
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    Nature Publishing Group (NPG)
    Publication Date: 2014-01-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Muller-Landau, Helene C -- England -- Nature. 2014 Feb 6;506(7486):44-5. doi: 10.1038/nature12851. Epub 2014 Jan 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Smithsonian Tropical Research Institute, Apartado Postal 0843-03092, Panama City, Panama.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24463509" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biodiversity ; Fungi/*physiology ; *Herbivory ; Insects/*physiology ; Trees/*microbiology/*physiology
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  • 28
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    Nature Publishing Group (NPG)
    Publication Date: 2014-10-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Check Hayden, Erika -- England -- Nature. 2014 Oct 30;514(7524):546. doi: 10.1038/514546a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25355339" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*drug effects ; Animals ; Clinical Trials as Topic/*veterinary ; Dogs/*physiology ; Female ; Humans ; Longevity/*drug effects ; Male ; Mice ; Models, Animal ; Pets/*physiology ; Pilot Projects ; Sirolimus/administration & dosage/adverse effects/*pharmacology
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  • 29
    Publication Date: 2014-09-26
    Description: Retinoblastoma is a childhood retinal tumour that initiates in response to biallelic RB1 inactivation and loss of functional retinoblastoma (Rb) protein. Although Rb has diverse tumour-suppressor functions and is inactivated in many cancers, germline RB1 mutations predispose to retinoblastoma far more strongly than to other malignancies. This tropism suggests that retinal cell-type-specific circuitry sensitizes to Rb loss, yet the nature of the circuitry and the cell type in which it operates have been unclear. Here we show that post-mitotic human cone precursors are uniquely sensitive to Rb depletion. Rb knockdown induced cone precursor proliferation in prospectively isolated populations and in intact retina. Proliferation followed the induction of E2F-regulated genes, and depended on factors having strong expression in maturing cone precursors and crucial roles in retinoblastoma cell proliferation, including MYCN and MDM2. Proliferation of Rb-depleted cones and retinoblastoma cells also depended on the Rb-related protein p107, SKP2, and a p27 downregulation associated with cone precursor maturation. Moreover, Rb-depleted cone precursors formed tumours in orthotopic xenografts with histological features and protein expression typical of human retinoblastoma. These findings provide a compelling molecular rationale for a cone precursor origin of retinoblastoma. More generally, they demonstrate that cell-type-specific circuitry can collaborate with an initiating oncogenic mutation to enable tumorigenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4232224/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4232224/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xu, Xiaoliang L -- Singh, Hardeep P -- Wang, Lu -- Qi, Dong-Lai -- Poulos, Bradford K -- Abramson, David H -- Jhanwar, Suresh C -- Cobrinik, David -- 1R01CA137124/CA/NCI NIH HHS/ -- R01 CA137124/CA/NCI NIH HHS/ -- England -- Nature. 2014 Oct 16;514(7522):385-8. doi: 10.1038/nature13813. Epub 2014 Sep 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Pathology, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, New York 10021, USA [2] Sloan-Kettering Institute for Cancer Research, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, New York 10021, USA. ; 1] The Vision Center, Division of Ophthalmology, Department of Surgery, Children's Hospital Los Angeles, 4650 Sunset Boulevard, Los Angeles, California 90027, USA [2] The Saban Research Institute, Children's Hospital Los Angeles, 4650 Sunset Boulevard, Los Angeles, California 90027, USA. ; Department of Pathology, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, New York 10021, USA. ; Department of Pathology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, New York 10461, USA. ; Ophthalmic Oncology Service, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, New York 10021, USA. ; 1] Department of Pathology, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, New York 10021, USA [2] Department of Medicine, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, New York 10021, USA. ; 1] The Vision Center, Division of Ophthalmology, Department of Surgery, Children's Hospital Los Angeles, 4650 Sunset Boulevard, Los Angeles, California 90027, USA [2] The Saban Research Institute, Children's Hospital Los Angeles, 4650 Sunset Boulevard, Los Angeles, California 90027, USA [3] USC Eye Institute, Department of Ophthalmology, Keck School of Medicine of the University of Southern California, 1450 San Pablo Street, Los Angeles, California 90033, USA [4] Norris Comprehensive Cancer Center, Keck School of Medicine of the University of Southern California, 1441 Eastlake Avenue, Los Angeles, California 90033, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25252974" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Transformation, Neoplastic ; E2F Transcription Factors/metabolism ; Gene Expression Regulation, Neoplastic ; Genes, Retinoblastoma/genetics ; Heterografts ; Humans ; Nuclear Proteins/metabolism ; Oncogene Proteins/metabolism ; Organ Specificity ; Proto-Oncogene Proteins c-mdm2/metabolism ; Retinal Cone Photoreceptor Cells/*metabolism/*pathology ; Retinoblastoma/genetics/*metabolism/*pathology ; Retinoblastoma Protein/deficiency/genetics/*metabolism ; Retinoblastoma-Like Protein p107/metabolism ; Retinoblastoma-Like Protein p130/deficiency/metabolism ; S-Phase Kinase-Associated Proteins/metabolism ; Stem Cells/metabolism/pathology
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  • 30
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    Nature Publishing Group (NPG)
    Publication Date: 2014-10-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roberge, Aki -- England -- Nature. 2014 Oct 23;514(7523):440-1. doi: 10.1038/514440a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉NASA Goddard Space Flight Center, Exoplanets and Stellar Astrophysics Laboratory, Greenbelt, Maryland 20771, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25341780" target="_blank"〉PubMed〈/a〉
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  • 31
    Publication Date: 2014-11-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tallis, Heather -- Lubchenco, Jane -- England -- Nature. 2014 Nov 6;515(7525):27-8. doi: 10.1038/515027a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Nature Conservancy in Santa Cruz, California, USA. ; Oregon State University in Corvallis, Oregon, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25373659" target="_blank"〉PubMed〈/a〉
    Keywords: *Conservation of Natural Resources/economics/methods/trends ; Ecology/economics/trends ; *Environmental Policy/economics/trends ; *Goals
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  • 32
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    Nature Publishing Group (NPG)
    Publication Date: 2014-10-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Check Hayden, Erika -- England -- Nature. 2014 Oct 16;514(7522):282. doi: 10.1038/514282a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25318499" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; *Databases, Genetic ; Disease/*genetics ; Genetic Association Studies ; Genetic Variation/genetics ; Genetics, Medical ; Humans ; Information Dissemination ; Phenotype ; Sequence Analysis, DNA
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  • 33
    Publication Date: 2014-09-06
    Description: Post-transcriptional modification of RNA nucleosides occurs in all living organisms. Pseudouridine, the most abundant modified nucleoside in non-coding RNAs, enhances the function of transfer RNA and ribosomal RNA by stabilizing the RNA structure. Messenger RNAs were not known to contain pseudouridine, but artificial pseudouridylation dramatically affects mRNA function--it changes the genetic code by facilitating non-canonical base pairing in the ribosome decoding centre. However, without evidence of naturally occurring mRNA pseudouridylation, its physiological relevance was unclear. Here we present a comprehensive analysis of pseudouridylation in Saccharomyces cerevisiae and human RNAs using Pseudo-seq, a genome-wide, single-nucleotide-resolution method for pseudouridine identification. Pseudo-seq accurately identifies known modification sites as well as many novel sites in non-coding RNAs, and reveals hundreds of pseudouridylated sites in mRNAs. Genetic analysis allowed us to assign most of the new modification sites to one of seven conserved pseudouridine synthases, Pus1-4, 6, 7 and 9. Notably, the majority of pseudouridines in mRNA are regulated in response to environmental signals, such as nutrient deprivation in yeast and serum starvation in human cells. These results suggest a mechanism for the rapid and regulated rewiring of the genetic code through inducible mRNA modifications. Our findings reveal unanticipated roles for pseudouridylation and provide a resource for identifying the targets of pseudouridine synthases implicated in human disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4224642/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4224642/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carlile, Thomas M -- Rojas-Duran, Maria F -- Zinshteyn, Boris -- Shin, Hakyung -- Bartoli, Kristen M -- Gilbert, Wendy V -- GM081399/GM/NIGMS NIH HHS/ -- GM094303/GM/NIGMS NIH HHS/ -- R00 GM081399/GM/NIGMS NIH HHS/ -- R01 GM094303/GM/NIGMS NIH HHS/ -- R01 GM101316/GM/NIGMS NIH HHS/ -- T32 GM007287/GM/NIGMS NIH HHS/ -- T32GM007287/GM/NIGMS NIH HHS/ -- England -- Nature. 2014 Nov 6;515(7525):143-6. doi: 10.1038/nature13802. Epub 2014 Sep 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25192136" target="_blank"〉PubMed〈/a〉
    Keywords: Base Composition ; Food Deprivation ; Genetic Code ; Genome/genetics ; Humans ; Intramolecular Transferases/metabolism ; Pseudouridine/*analysis/chemistry/genetics ; RNA, Messenger/*chemistry/metabolism ; RNA, Untranslated/chemistry ; Saccharomyces cerevisiae/cytology/*genetics ; Sequence Analysis, RNA
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  • 34
    Publication Date: 2014-01-31
    Description: The clustered regularly interspaced short palindromic repeats (CRISPR)-associated enzyme Cas9 is an RNA-guided endonuclease that uses RNA-DNA base-pairing to target foreign DNA in bacteria. Cas9-guide RNA complexes are also effective genome engineering agents in animals and plants. Here we use single-molecule and bulk biochemical experiments to determine how Cas9-RNA interrogates DNA to find specific cleavage sites. We show that both binding and cleavage of DNA by Cas9-RNA require recognition of a short trinucleotide protospacer adjacent motif (PAM). Non-target DNA binding affinity scales with PAM density, and sequences fully complementary to the guide RNA but lacking a nearby PAM are ignored by Cas9-RNA. Competition assays provide evidence that DNA strand separation and RNA-DNA heteroduplex formation initiate at the PAM and proceed directionally towards the distal end of the target sequence. Furthermore, PAM interactions trigger Cas9 catalytic activity. These results reveal how Cas9 uses PAM recognition to quickly identify potential target sites while scanning large DNA molecules, and to regulate scission of double-stranded DNA.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4106473/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4106473/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sternberg, Samuel H -- Redding, Sy -- Jinek, Martin -- Greene, Eric C -- Doudna, Jennifer A -- GM074739/GM/NIGMS NIH HHS/ -- R01 GM073794/GM/NIGMS NIH HHS/ -- R01 GM074739/GM/NIGMS NIH HHS/ -- T32 GM066698/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 Mar 6;507(7490):62-7. doi: 10.1038/nature13011. Epub 2014 Jan 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Chemistry, University of California, Berkeley, California 94720, USA [2]. ; 1] Department of Chemistry, Columbia University, New York, New York 10032, USA [2]. ; 1] Howard Hughes Medical Institute, University of California, Berkeley, California 94720, USA [2] Department of Biochemistry, University of Zurich, 8057 Zurich, Switzerland. ; Department of Biochemistry and Molecular Biophysics and Howard Hughes Medical Institute, Columbia University, New York, New York 10032, USA. ; 1] Department of Chemistry, University of California, Berkeley, California 94720, USA [2] Howard Hughes Medical Institute, University of California, Berkeley, California 94720, USA [3] Department of Molecular and Cell Biology, University of California, Berkeley, California 94720, USA [4] Physical Biosciences Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24476820" target="_blank"〉PubMed〈/a〉
    Keywords: Apoenzymes/metabolism ; *Base Pairing ; Base Sequence ; Biocatalysis ; CRISPR-Associated Proteins/*metabolism ; *CRISPR-Cas Systems ; Clustered Regularly Interspaced Short Palindromic Repeats/*genetics ; DNA/chemistry/genetics/metabolism ; *DNA Cleavage ; Diffusion ; Endonucleases/*metabolism ; Enzyme Activation ; Genetic Engineering/methods ; Genome/genetics ; Nucleic Acid Denaturation ; Nucleic Acid Heteroduplexes/chemistry/genetics/metabolism ; Nucleotide Motifs ; RNA/chemistry/*genetics/metabolism ; Streptococcus pyogenes/enzymology/immunology ; Substrate Specificity ; Thermodynamics
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  • 35
    Publication Date: 2014-09-05
    Description: Receptor interacting protein kinase 1 (RIPK1) has an essential role in the signalling triggered by death receptors and pattern recognition receptors. RIPK1 is believed to function as a node driving NF-kappaB-mediated cell survival and inflammation as well as caspase-8 (CASP8)-dependent apoptotic or RIPK3/MLKL-dependent necroptotic cell death. The physiological relevance of this dual function has remained elusive because of the perinatal death of RIPK1 full knockout mice. To circumvent this problem, we generated RIPK1 conditional knockout mice, and show that mice lacking RIPK1 in intestinal epithelial cells (IECs) spontaneously develop severe intestinal inflammation associated with IEC apoptosis leading to early death. This early lethality was rescued by antibiotic treatment, MYD88 deficiency or tumour-necrosis factor (TNF) receptor 1 deficiency, demonstrating the importance of commensal bacteria and TNF in the IEC Ripk1 knockout phenotype. CASP8 deficiency, but not RIPK3 deficiency, rescued the inflammatory phenotype completely, indicating the indispensable role of RIPK1 in suppressing CASP8-dependent apoptosis but not RIPK3-dependent necroptosis in the intestine. RIPK1 kinase-dead knock-in mice did not exhibit any sign of inflammation, suggesting that RIPK1-mediated protection resides in its kinase-independent platform function. Depletion of RIPK1 in intestinal organoid cultures sensitized them to TNF-induced apoptosis, confirming the in vivo observations. Unexpectedly, TNF-mediated NF-kappaB activation remained intact in these organoids. Our results demonstrate that RIPK1 is essential for survival of IECs, ensuring epithelial homeostasis by protecting the epithelium from CASP8-mediated IEC apoptosis independently of its kinase activity and NF-kappaB activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takahashi, Nozomi -- Vereecke, Lars -- Bertrand, Mathieu J M -- Duprez, Linde -- Berger, Scott B -- Divert, Tatyana -- Goncalves, Amanda -- Sze, Mozes -- Gilbert, Barbara -- Kourula, Stephanie -- Goossens, Vera -- Lefebvre, Sylvie -- Gunther, Claudia -- Becker, Christoph -- Bertin, John -- Gough, Peter J -- Declercq, Wim -- van Loo, Geert -- Vandenabeele, Peter -- England -- Nature. 2014 Sep 4;513(7516):95-9. doi: 10.1038/nature13706.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] VIB Inflammation Research Center, Technologiepark 927, B-9052 Ghent, Belgium [2] Department of Biomedical Molecular Biology, Ghent University, Technologiepark 927, B-9052 Ghent, Belgium. ; Pattern Recognition Receptor Discovery Performance Unit, Immuno-inflammation Therapeutic Area, GlaxoSmithKline, Collegeville, Pennsylvania 19426, USA. ; 1] VIB Inflammation Research Center, Technologiepark 927, B-9052 Ghent, Belgium [2] Department of Biomedical Molecular Biology, Ghent University, Technologiepark 927, B-9052 Ghent, Belgium [3] VIB Bio Imaging Core Gent, Technologiepark 927, B-9052 Ghent, Belgium. ; Department of Medicine 1, Friedrich-Alexander-University, D-91054 Erlangen, Germany. ; 1] VIB Inflammation Research Center, Technologiepark 927, B-9052 Ghent, Belgium [2] Department of Biomedical Molecular Biology, Ghent University, Technologiepark 927, B-9052 Ghent, Belgium [3] Methusalem program, Ghent University, Technologiepark 927, B-9052 Ghent, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25186904" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Bacterial Agents/pharmacology ; *Apoptosis/drug effects ; Caspase 8/genetics/metabolism ; Cell Survival/drug effects ; Epithelial Cells/*cytology/drug effects/*metabolism/pathology ; Epithelium/drug effects/*metabolism/pathology ; Female ; Gene Deletion ; *Homeostasis/drug effects ; Inflammation/metabolism/pathology ; Intestines/*cytology/drug effects/*metabolism/pathology ; Male ; Mice ; Mice, Knockout ; Myeloid Differentiation Factor 88/deficiency ; NF-kappa B/metabolism ; Necrosis ; Organoids/cytology/drug effects/enzymology/metabolism ; Protein Kinases/metabolism ; Receptor-Interacting Protein Serine-Threonine ; Kinases/deficiency/genetics/*metabolism ; Receptors, Tumor Necrosis Factor, Type I/deficiency ; Survival Analysis ; Tumor Necrosis Factors/pharmacology
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  • 36
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    Nature Publishing Group (NPG)
    Publication Date: 2014-11-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rivers, Caitlin -- England -- Nature. 2014 Nov 27;515(7528):492. doi: 10.1038/515492a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Virginia Bioinformatics Institute, Virginia Tech, Blacksburg, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25428492" target="_blank"〉PubMed〈/a〉
    Keywords: Disease Outbreaks/*statistics & numerical data ; Hemorrhagic Fever, Ebola/*epidemiology/*transmission ; Humans ; *Models, Biological
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  • 37
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    Nature Publishing Group (NPG)
    Publication Date: 2014-02-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Herrmann, Mark -- England -- Nature. 2014 Feb 20;506(7488):302-3. doi: 10.1038/nature13057. Epub 2014 Feb 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Pulsed Power Sciences Center, Sandia National Laboratories, Albuquerque, New Mexico 87185, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24522529" target="_blank"〉PubMed〈/a〉
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  • 38
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    Nature Publishing Group (NPG)
    Publication Date: 2014-10-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Check Hayden, Erika -- England -- Nature. 2014 Oct 30;514(7524):554-7. doi: 10.1038/514554a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25355344" target="_blank"〉PubMed〈/a〉
    Keywords: Africa, Western/epidemiology ; Animals ; Chiroptera/virology ; Disease Outbreaks/*statistics & numerical data ; Disease Reservoirs/*virology ; Ebolavirus/*isolation & purification/*pathogenicity/physiology ; Global Health ; Hemorrhagic Fever, Ebola/*epidemiology/immunology/therapy/*virology ; Humans ; Immunity, Innate ; Primates/virology ; Survival Rate ; Swine/virology ; Virology
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  • 39
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    Nature Publishing Group (NPG)
    Publication Date: 2014-11-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carri, Maria Teresa -- England -- Nature. 2014 Nov 20;515(7527):343. doi: 10.1038/515343e.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Rome 'Tor Vergata', Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25409816" target="_blank"〉PubMed〈/a〉
    Keywords: Amyotrophic Lateral Sclerosis/*economics ; Animals ; Biomedical Research/*economics ; Fund Raising/*methods ; Humans ; *Public Opinion
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  • 40
    Publication Date: 2014-08-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takeuchi, Tomonori -- Morris, Richard G M -- England -- Nature. 2014 Sep 18;513(7518):323-4. doi: 10.1038/nature13745. Epub 2014 Aug 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Cognitive and Neural Systems, University of Edinburgh, Edinburgh EH8 9JZ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25162529" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Hippocampus/*physiology ; Male ; Memory/*physiology
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  • 41
    Publication Date: 2014-09-26
    Description: The formation of branched lariat RNA is an evolutionarily conserved feature of splicing reactions for both group II and spliceosomal introns. The lariat is important for the fidelity of 5' splice-site selection and consists of a 2'-5' phosphodiester bond between a bulged adenosine and the 5' end of the intron. To gain insight into this ubiquitous intramolecular linkage, we determined the crystal structure of a eukaryotic group IIB intron in the lariat form at 3.7 A. This revealed that two tandem tetraloop-receptor interactions, eta-eta' and pi-pi', place domain VI in the core to position the lariat bond in the post-catalytic state. On the basis of structural and biochemical data, we propose that pi-pi' is a dynamic interaction that mediates the transition between the two steps of splicing, with eta-eta' serving an ancillary role. The structure also reveals a four-magnesium-ion cluster involved in both catalysis and positioning of the 5' end. Given the evolutionary relationship between group II and nuclear introns, it is likely that this active site configuration exists in the spliceosome as well.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4197185/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4197185/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Robart, Aaron R -- Chan, Russell T -- Peters, Jessica K -- Rajashankar, Kanagalaghatta R -- Toor, Navtej -- 5R01GM102216/GM/NIGMS NIH HHS/ -- 5T32GM007240/GM/NIGMS NIH HHS/ -- 5T32GM008326/GM/NIGMS NIH HHS/ -- 8P41GM103403-10/GM/NIGMS NIH HHS/ -- P41 GM103403/GM/NIGMS NIH HHS/ -- R01 GM102216/GM/NIGMS NIH HHS/ -- T32 GM007240/GM/NIGMS NIH HHS/ -- T32 GM008326/GM/NIGMS NIH HHS/ -- England -- Nature. 2014 Oct 9;514(7521):193-7. doi: 10.1038/nature13790. Epub 2014 Sep 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Biochemistry, University of California, San Diego, La Jolla, California 92093, USA. ; NE-CAT and Department of Chemistry and Chemical Biology, Cornell University, Argonne National Laboratory, Argonne, Illinois 60439, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25252982" target="_blank"〉PubMed〈/a〉
    Keywords: Biocatalysis ; Catalytic Domain ; Crystallography, X-Ray ; Evolution, Molecular ; *Introns/genetics ; Magnesium/metabolism/pharmacology ; Models, Molecular ; *Nucleic Acid Conformation/drug effects ; *Phaeophyta/chemistry/genetics ; RNA Splicing/genetics ; Ribosome Subunits, Large/genetics ; Spliceosomes/chemistry
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  • 42
    Publication Date: 2014-09-26
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4476531/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4476531/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fieni, Francesca -- Johnson, Derrick E -- Hudmon, Andy -- Kirichok, Yuriy -- R01 NS078171/NS/NINDS NIH HHS/ -- England -- Nature. 2014 Sep 25;513(7519):E1-2. doi: 10.1038/nature13626.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of California San Francisco, San Francisco, California 94158, USA. ; Department of Biochemistry and Molecular Biology, Stark Neuroscience Research Institute, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25254480" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/*metabolism ; Female ; Mitochondria, Heart/*metabolism/*pathology ; Myocardium/*enzymology/*pathology ; *Stress, Physiological
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  • 43
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    Nature Publishing Group (NPG)
    Publication Date: 2014-11-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anthes, Emily -- England -- Nature. 2014 Nov 13;515(7526):185-7. doi: 10.1038/515185a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25391944" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/physiology/physiopathology ; Antidepressive Agents/therapeutic use ; Brain Mapping ; *Cognitive Therapy ; Confounding Factors (Epidemiology) ; Depression/genetics/physiopathology/*psychology/*therapy ; Depressive Disorder/genetics/physiopathology/psychology/therapy ; Female ; Humans ; Magnetic Resonance Imaging ; Prefrontal Cortex/physiology/physiopathology ; Prognosis ; Treatment Outcome
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  • 44
    Publication Date: 2014-10-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rodell, Christopher B -- Burdick, Jason A -- England -- Nature. 2014 Oct 30;514(7524):574-5. doi: 10.1038/514574a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bioengineering, School of Engineering and Applied Science, University of Pennsylvania, Philadelphia 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25355357" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Magnetics/*methods ; Nanotechnology/*methods ; Tissue Engineering/*methods
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  • 45
    Publication Date: 2014-04-18
    Description: Trisomy 21 is the most frequent genetic cause of cognitive impairment. To assess the perturbations of gene expression in trisomy 21, and to eliminate the noise of genomic variability, we studied the transcriptome of fetal fibroblasts from a pair of monozygotic twins discordant for trisomy 21. Here we show that the differential expression between the twins is organized in domains along all chromosomes that are either upregulated or downregulated. These gene expression dysregulation domains (GEDDs) can be defined by the expression level of their gene content, and are well conserved in induced pluripotent stem cells derived from the twins' fibroblasts. Comparison of the transcriptome of the Ts65Dn mouse model of Down's syndrome and normal littermate mouse fibroblasts also showed GEDDs along the mouse chromosomes that were syntenic in human. The GEDDs correlate with the lamina-associated (LADs) and replication domains of mammalian cells. The overall position of LADs was not altered in trisomic cells; however, the H3K4me3 profile of the trisomic fibroblasts was modified and accurately followed the GEDD pattern. These results indicate that the nuclear compartments of trisomic cells undergo modifications of the chromatin environment influencing the overall transcriptome, and that GEDDs may therefore contribute to some trisomy 21 phenotypes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Letourneau, Audrey -- Santoni, Federico A -- Bonilla, Ximena -- Sailani, M Reza -- Gonzalez, David -- Kind, Jop -- Chevalier, Claire -- Thurman, Robert -- Sandstrom, Richard S -- Hibaoui, Youssef -- Garieri, Marco -- Popadin, Konstantin -- Falconnet, Emilie -- Gagnebin, Maryline -- Gehrig, Corinne -- Vannier, Anne -- Guipponi, Michel -- Farinelli, Laurent -- Robyr, Daniel -- Migliavacca, Eugenia -- Borel, Christelle -- Deutsch, Samuel -- Feki, Anis -- Stamatoyannopoulos, John A -- Herault, Yann -- van Steensel, Bas -- Guigo, Roderic -- Antonarakis, Stylianos E -- U54HG007010/HG/NHGRI NIH HHS/ -- England -- Nature. 2014 Apr 17;508(7496):345-50. doi: 10.1038/nature13200.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Genetic Medicine and Development, University of Geneva Medical School, University Hospitals of Geneva, 1211 Geneva, Switzerland [2]. ; Department of Genetic Medicine and Development, University of Geneva Medical School, University Hospitals of Geneva, 1211 Geneva, Switzerland. ; Center for Genomic Regulation, University Pompeu Fabra, 08003 Barcelona, Spain. ; Division of Gene Regulation, Netherlands Cancer Institute, 1066 CX Amsterdam, The Netherlands. ; AneuPath 21, Institut de Genetique Biologie Moleculaire et Cellulaire, Translational medicine and Neuroscience program, IGBMC, ICS, PHENOMIN, CNRS, INSERM, Universite de Strasbourg, UMR7104, UMR964, 1 rue Laurent Fries, 67404 Illkirch, France. ; Department of Genome Sciences, University of Washington, Seattle, Washington 98195, USA. ; Stem Cell Research Laboratory, Department of Obstetrics and Gynecology, Geneva University Hospitals, 1211 Geneva, Switzerland. ; FASTERIS SA, 1228 Plan-les-Ouates, Switzerland. ; 1] Department of Genetic Medicine and Development, University of Geneva Medical School, University Hospitals of Geneva, 1211 Geneva, Switzerland [2] Swiss Institute of Bioinfomatics, 1211 Geneva, Switzerland. ; DOE Joint Genome Institute, Walnut Creek, California 94598, USA. ; 1] Department of Genetic Medicine and Development, University of Geneva Medical School, University Hospitals of Geneva, 1211 Geneva, Switzerland [2] iGE3 Institute of Genetics and Genomics of Geneva, 1211 Geneva, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24740065" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Chromatin/chemistry/metabolism ; Chromosomes, Human, Pair 21/genetics ; Chromosomes, Mammalian/genetics ; DNA Replication Timing ; Down Syndrome/*genetics/pathology ; Female ; Fetus/cytology ; Fibroblasts ; Gene Expression Regulation/*genetics ; Genome/*genetics ; Histones/chemistry/metabolism ; Humans ; Induced Pluripotent Stem Cells/metabolism ; Lysine/metabolism ; Male ; Methylation ; Mice ; Transcriptome/*genetics ; Twins, Monozygotic/genetics
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  • 46
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    Nature Publishing Group (NPG)
    Publication Date: 2014-04-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heremans, Joseph P -- England -- Nature. 2014 Apr 17;508(7496):327-8. doi: 10.1038/508327a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Mechanical and Aerospace Engineering and of Physics, Ohio State University, Columbus, Ohio 43210, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24740062" target="_blank"〉PubMed〈/a〉
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  • 47
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    Nature Publishing Group (NPG)
    Publication Date: 2014-09-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wulder, Michael A -- Coops, Nicholas C -- England -- Nature. 2014 Sep 4;513(7516):30-1. doi: 10.1038/513030a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Canadian Forest Service, Natural Resources Canada, Victoria, Canada. ; Faculty of Forest Resources Management, University of British Columbia, Vancouver, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25186885" target="_blank"〉PubMed〈/a〉
    Keywords: *Access to Information ; *Earth (Planet) ; *Environmental Monitoring/economics/instrumentation ; Policy Making ; *Satellite Imagery/economics
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  • 48
    Publication Date: 2014-04-04
    Description: In the mammalian cerebral cortex, neural responses are highly variable during spontaneous activity and sensory stimulation. To explain this variability, the cortex of alert animals has been proposed to be in an asynchronous high-conductance state in which irregular spiking arises from the convergence of large numbers of uncorrelated excitatory and inhibitory inputs onto individual neurons. Signatures of this state are that a neuron's membrane potential (Vm) hovers just below spike threshold, and its aggregate synaptic input is nearly Gaussian, arising from many uncorrelated inputs. Alternatively, irregular spiking could arise from infrequent correlated input events that elicit large fluctuations in Vm (refs 5, 6). To distinguish between these hypotheses, we developed a technique to perform whole-cell Vm measurements from the cortex of behaving monkeys, focusing on primary visual cortex (V1) of monkeys performing a visual fixation task. Here we show that, contrary to the predictions of an asynchronous state, mean Vm during fixation was far from threshold (14 mV) and spiking was triggered by occasional large spontaneous fluctuations. Distributions of Vm values were skewed beyond that expected for a range of Gaussian input, but were consistent with synaptic input arising from infrequent correlated events. Furthermore, spontaneous fluctuations in Vm were correlated with the surrounding network activity, as reflected in simultaneously recorded nearby local field potential. Visual stimulation, however, led to responses more consistent with an asynchronous state: mean Vm approached threshold, fluctuations became more Gaussian, and correlations between single neurons and the surrounding network were disrupted. These observations show that sensory drive can shift a common cortical circuitry from a synchronous to an asynchronous state.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4067243/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4067243/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tan, Andrew Y Y -- Chen, Yuzhi -- Scholl, Benjamin -- Seidemann, Eyal -- Priebe, Nicholas J -- EY-016454/EY/NEI NIH HHS/ -- EY-019288/EY/NEI NIH HHS/ -- EY-16752/EY/NEI NIH HHS/ -- R01 EY016454/EY/NEI NIH HHS/ -- R01 EY019288/EY/NEI NIH HHS/ -- T32 EY021462/EY/NEI NIH HHS/ -- England -- Nature. 2014 May 8;509(7499):226-9. doi: 10.1038/nature13159. Epub 2014 Mar 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Center for Perceptual Systems, University of Texas, Austin, Texas 78712, USA [2] Department of Neuroscience, College of Natural Sciences, University of Texas, Austin, Texas 78712, USA [3]. ; 1] Center for Perceptual Systems, University of Texas, Austin, Texas 78712, USA [2] Department of Neuroscience, College of Natural Sciences, University of Texas, Austin, Texas 78712, USA [3] Department of Psychology, University of Texas, Austin, Texas 78712, USA [4]. ; 1] Center for Perceptual Systems, University of Texas, Austin, Texas 78712, USA [2] Department of Neuroscience, College of Natural Sciences, University of Texas, Austin, Texas 78712, USA [3] Department of Psychology, University of Texas, Austin, Texas 78712, USA. ; 1] Center for Perceptual Systems, University of Texas, Austin, Texas 78712, USA [2] Department of Neuroscience, College of Natural Sciences, University of Texas, Austin, Texas 78712, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24695217" target="_blank"〉PubMed〈/a〉