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  • 1
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2017-03-03
    Description: Author: Jake Yeston
    Keywords: Organic Chemistry
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  • 2
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2017-02-10
    Description: Author: Jake Yeston
    Keywords: Inorganic Chemistry
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  • 3
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2017-04-14
    Description: Author: Jake Yeston
    Keywords: Organic Chemistry
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  • 4
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2017-04-14
    Description: The allotropes formed by carbon reflect differences in its bonding: single bonds in diamond, double bonds in graphite and graphene, and triple bonds in polyynes. Fashioning graphene sheets into bowls, monkey saddles, balls, and tubes has led to a number of molecular allotropes of carbon or carbon-rich quasi-allotropes with novel topologies and shapes. A simple ring of carbon can be reduced to practice in various forms (1): a cyclic array of carbon atoms, a “pearl necklace” of benzene rings, or a cylindrical hoop of flank-fused benzenes, just to name a few. On page 172 of this issue, Povie et al. (2) report on the synthesis of an angular-fused hoop structure, which has been a long-standing target. Author: Jay S. Siegel
    Keywords: Organic Chemistry
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  • 5
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2017-04-14
    Description: Author: Jake Yeston
    Keywords: Organic Chemistry
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  • 6
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2017-03-25
    Description: Author: L. Bryan Ray
    Keywords: Signal Transduction
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    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2017-01-27
    Description: Author: Jake Yeston
    Keywords: Inorganic Chemistry
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  • 8
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2017-03-03
    Description: Author: Jake Yeston
    Keywords: Organic Chemistry
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  • 9
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2017-04-01
    Description: Author: Jake Yeston
    Keywords: Organic Chemistry
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  • 10
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2017-01-27
    Description: Polynitrogens have the potential for ultrahigh-performing explosives or propellants because singly or doubly bonded polynitrogens can decompose to triply bonded dinitrogen (N2) with an extraordinarily large energy release. The large energy content and relatively low activation energy toward decomposition makes the synthesis of a stable polynitrogen allotrope an extraordinary challenge. Many elements exist in different forms (allotropes)—for example, carbon can exist as graphite, diamond, buckyballs, or graphene. However, no stable neutral allotropes are known for nitrogen, and only two stable homonuclear polynitrogen ions had been isolated until now—namely, the N3− anion (1) and the N5+ cation (2). On page 374 of this issue, Zhang et al. (3) report the synthesis and characterization of the first stable salt of the cyclo-N5− anion, only the third stable homonuclear polynitrogen ion ever isolated. Author: Karl O. Christe
    Keywords: Inorganic Chemistry
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  • 11
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2017-01-13
    Description: Author: Jake Yeston
    Keywords: Organic Chemistry
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  • 12
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2016-07-08
    Description: Author: Phil Szuromi
    Keywords: Organic Chemistry
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  • 13
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2016-07-08
    Description: Author: Jake Yeston
    Keywords: Organic Chemistry
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  • 14
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2016-05-27
    Description: Author: Jake Yeston
    Keywords: Organic Chemistry
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  • 15
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2016-07-15
    Description: Author: Jake Yeston
    Keywords: Organic Chemistry
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  • 16
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2016-07-22
    Description: Author: Jake Yeston
    Keywords: Organic Chemistry
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  • 17
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2016-06-24
    Description: Author: Jake Yeston
    Keywords: Organic Chemistry
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  • 18
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2016-07-01
    Description: Author: Jake Yeston
    Keywords: Organic Chemistry
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  • 19
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2016-06-10
    Description: Transition metal–catalyzed arylation of C–H bonds has been intensively studied for forming C–C bonds in complex-molecule synthesis (1). An acidic C–H bond (for example, one near a double bond or an O atom) is cleaved to form a carbon–metal bond, which then couples to arene. Many of these organometallic species can be generated catalytically. Much less research has dealt with unreactive nonacidic sp3 C–H bond functionalization (3). On page 1304 of this issue, Shaw et al. (3) report an efficient and general method that focuses on arylation of sp3 C–H bonds at carbon atoms adjacent to amines and to cyclic ethers by combining nickel, visible-light photoredox, and hydrogen-atom transfer (HAT) catalysis. Author: Corinne Fruit
    Keywords: Organic Chemistry
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  • 20
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2016-06-10
    Description: Author: Jake Yeston
    Keywords: Organic Chemistry
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  • 21
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2016-09-09
    Description: Author: Jake Yeston
    Keywords: Organic Chemistry
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  • 22
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2016-09-03
    Description: Author: L. Bryan Ray
    Keywords: Signal Transduction
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  • 23
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2016-09-07
    Description: Author: Jake Yeston
    Keywords: Organic Chemistry
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  • 24
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2016-05-20
    Description: Antibiotics have been taking it on the chin lately. Not only has resistance to the anti-infective medications been growing, but drug companies have been dropping antibiotic research programs, because the drugs are difficult and expensive to make. Now, new help is on the way. Researchers report this week that they've found a way to churn out new members of one of the most widely used classes of antibiotics. These drugs, called macrolides, were first developed in the 1950s and now represent a major bulwark against infections. A bevy of possible new drugs in this class could lead to new weapons against antibiotic-resistant infections, and possibly save millions of lives. Author: Robert F. Service
    Keywords: Organic Chemistry
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  • 25
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2016-05-20
    Description: Author: L. Bryan Ray
    Keywords: Signal Transduction
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  • 26
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2016-04-22
    Description: Author: Jake Yeston
    Keywords: Organic Chemistry
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  • 27
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2016-04-29
    Description: Author: Jake Yeston
    Keywords: Organic Chemistry
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  • 28
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2016-05-13
    Description: Author: Jake Yeston
    Keywords: Organic Chemistry
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  • 29
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2016-04-29
    Description: Author: L. Bryan Ray
    Keywords: Signal Transduction
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  • 30
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2016-04-01
    Description: The SN2 nucleophilic substitution reaction, X− + RY → XR + Y−, is a paradigm reaction in organic chemistry (1). The modern understanding of the SN2 reaction mechanism is based on work of Hughes and Ingold (2), who proposed that the nucleophile (X−) approaches the carbon atom that bears the leaving group (Y−). As a result, the bond between the carbon atom and the leaving group becomes weakened. As this bond breaks and a new bond forms between the nucleophile and the carbon atom, the configuration of the carbon atom is inverted. Analyses of gas-phase reaction rates led to the suggestion of a potential energy surface (PES) with two wells connected by a central barrier transition state (3). Electronic structure calculations have confirmed this picture for some SN2 reactions (4), but recent studies have shown that the actual reaction dynamics may be considerably more complex (see the figure) (5–8). Authors: Jing Xie, William L. Hase
    Keywords: Organic Chemistry
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  • 31
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2016-04-01
    Description: Author: Julia Fahrenkamp-Uppenbrink
    Keywords: Organic Chemistry
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  • 32
    Publication Date: 2016-04-09
    Description: Activation of various cell surface receptors triggers the reorganization of downstream signaling molecules into micrometer- or submicrometer-sized clusters. However, the functional consequences of such clustering have been unclear. We biochemically reconstituted a 12-component signaling pathway on model membranes, beginning with T cell receptor (TCR) activation and ending with actin assembly. When TCR phosphorylation was triggered, downstream signaling proteins spontaneously separated into liquid-like clusters that promoted signaling outputs both in vitro and in human Jurkat T cells. Reconstituted clusters were enriched in kinases but excluded phosphatases and enhanced actin filament assembly by recruiting and organizing actin regulators. These results demonstrate that protein phase separation can create a distinct physical and biochemical compartment that facilitates signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Su, Xiaolei -- Ditlev, Jonathon A -- Hui, Enfu -- Xing, Wenmin -- Banjade, Sudeep -- Okrut, Julia -- King, David S -- Taunton, Jack -- Rosen, Michael K -- Vale, Ronald D -- 5-F32-DK101188/DK/NIDDK NIH HHS/ -- F32 DK101188/DK/NIDDK NIH HHS/ -- R01 GM056322/GM/NIGMS NIH HHS/ -- R01-GM56322/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):595-9. doi: 10.1126/science.aad9964. Epub 2016 Apr 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute (HHMI) Summer Institute, Marine Biological Laboratory, Woods Hole, MA 02543, USA. Department of Cellular and Molecular Pharmacology and Howard Hughes Medical Institute, University of California, San Francisco, CA 94158, USA. ; Howard Hughes Medical Institute (HHMI) Summer Institute, Marine Biological Laboratory, Woods Hole, MA 02543, USA. Department of Biophysics and Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. ; HHMI Mass Spectrometry Laboratory and Department of Molecular and Cellular Biology, University of California, Berkeley, CA 94720, USA. ; Howard Hughes Medical Institute (HHMI) Summer Institute, Marine Biological Laboratory, Woods Hole, MA 02543, USA. Department of Biophysics and Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. ron.vale@ucsf.edu michael.rosen@utsouthwestern.edu. ; Howard Hughes Medical Institute (HHMI) Summer Institute, Marine Biological Laboratory, Woods Hole, MA 02543, USA. Department of Cellular and Molecular Pharmacology and Howard Hughes Medical Institute, University of California, San Francisco, CA 94158, USA. ron.vale@ucsf.edu michael.rosen@utsouthwestern.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27056844" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/*metabolism ; Adaptor Proteins, Signal Transducing/*metabolism ; Fluorescence Recovery After Photobleaching ; Humans ; Jurkat Cells ; Membrane Proteins/*metabolism ; Mitogen-Activated Protein Kinase Kinases ; Phosphorylation ; Polymerization ; Receptors, Antigen, T-Cell/*agonists ; Signal Transduction ; T-Lymphocytes/*metabolism
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  • 33
    Publication Date: 2016-03-19
    Description: Systemic inflammation, which results from the massive release of proinflammatory molecules into the circulatory system, is a major risk factor for severe illness, but the precise mechanisms underlying its control are not fully understood. We observed that prostaglandin E2 (PGE2), through its receptor EP4, is down-regulated in human systemic inflammatory disease. Mice with reduced PGE2 synthesis develop systemic inflammation, associated with translocation of gut bacteria, which can be prevented by treatment with EP4 agonists. Mechanistically, we demonstrate that PGE2-EP4 signaling acts directly on type 3 innate lymphoid cells (ILCs), promoting their homeostasis and driving them to produce interleukin-22 (IL-22). Disruption of the ILC-IL-22 axis impairs PGE2-mediated inhibition of systemic inflammation. Hence, the ILC-IL-22 axis is essential in protecting against gut barrier dysfunction, enabling PGE2-EP4 signaling to impede systemic inflammation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4841390/" 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/PMC4841390/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duffin, Rodger -- O'Connor, Richard A -- Crittenden, Siobhan -- Forster, Thorsten -- Yu, Cunjing -- Zheng, Xiaozhong -- Smyth, Danielle -- Robb, Calum T -- Rossi, Fiona -- Skouras, Christos -- Tang, Shaohui -- Richards, James -- Pellicoro, Antonella -- Weller, Richard B -- Breyer, Richard M -- Mole, Damian J -- Iredale, John P -- Anderton, Stephen M -- Narumiya, Shuh -- Maizels, Rick M -- Ghazal, Peter -- Howie, Sarah E -- Rossi, Adriano G -- Yao, Chengcan -- 106122/Wellcome Trust/United Kingdom -- BB/K091121/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- DK37097/DK/NIDDK NIH HHS/ -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2016 Mar 18;351(6279):1333-8. doi: 10.1126/science.aad9903.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council (MRC) Centre for Inflammation Research, Queen's Medical Research Institute, The University of Edinburgh, Edinburgh EH16 4TJ, UK. ; Division of Pathway Medicine, Edinburgh Infectious Diseases, The University of Edinburgh, Edinburgh EH16 4SB, UK. ; Institute for Immunology and Infection Research, The University of Edinburgh, Edinburgh EH9 3JT, UK. ; MRC Centre for Regenerative Medicine, The University of Edinburgh, Edinburgh EH16 4UU, UK. ; Department of Gastroenterology, First Affiliated Hospital of Jinan University, Guangzhou 510630, China. ; Department of Veterans Affairs, Tennessee Valley Health Authority, Nashville, TN 37212, USA. Department of Medicine, Vanderbilt University Medical Center, Nashville, TN 37232, USA. ; Center for Innovation in Immunoregulative Technology and Therapeutics (AK Project), Kyoto University Graduate School of Medicine, Kyoto 606-8501, Japan. Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency (JST), Tokyo 102-0075, Japan. ; Division of Pathway Medicine, Edinburgh Infectious Diseases, The University of Edinburgh, Edinburgh EH16 4SB, UK. Centre for Synthetic and Systems Biology (SynthSys), The University of Edinburgh, Edinburgh EH9 3JD, UK. ; Medical Research Council (MRC) Centre for Inflammation Research, Queen's Medical Research Institute, The University of Edinburgh, Edinburgh EH16 4TJ, UK. chengcan.yao@ed.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26989254" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Infections/genetics/immunology ; Dinoprostone/*immunology ; Gene Expression ; Humans ; Immunity, Innate ; Inflammation/drug therapy/*immunology/microbiology ; Interleukins/*immunology ; Intestines/*immunology/microbiology ; Lymphocytes/*immunology ; Mice ; Receptors, Prostaglandin E, EP4 Subtype/antagonists & ; inhibitors/genetics/*immunology ; Signal Transduction
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  • 34
    Publication Date: 2016-01-23
    Description: Oligodendrocytes myelinate axons in the central nervous system and develop from oligodendrocyte precursor cells (OPCs) that must first migrate extensively during brain and spinal cord development. We show that OPCs require the vasculature as a physical substrate for migration. We observed that OPCs of the embryonic mouse brain and spinal cord, as well as the human cortex, emerge from progenitor domains and associate with the abluminal endothelial surface of nearby blood vessels. Migrating OPCs crawl along and jump between vessels. OPC migration in vivo was disrupted in mice with defective vascular architecture but was normal in mice lacking pericytes. Thus, physical interactions with the vascular endothelium are required for OPC migration. We identify Wnt-Cxcr4 (chemokine receptor 4) signaling in regulation of OPC-endothelial interactions and propose that this signaling coordinates OPC migration with differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tsai, Hui-Hsin -- Niu, Jianqin -- Munji, Roeben -- Davalos, Dimitrios -- Chang, Junlei -- Zhang, Haijing -- Tien, An-Chi -- Kuo, Calvin J -- Chan, Jonah R -- Daneman, Richard -- Fancy, Stephen P J -- 1P01 NS083513/NS/NINDS NIH HHS/ -- 1R01NS064517/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2016 Jan 22;351(6271):379-84. doi: 10.1126/science.aad3839.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, University of California at San Francisco (UCSF), San Francisco, CA 94158, USA. ; Departments of Pharmacology and Neuroscience, University of California at San Diego (UCSD), San Diego, CA 92093, USA. ; Department of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195, USA. ; Division of Hematology, Department of Medicine, Stanford University, Stanford, CA 94305, USA. ; Division of Hematology, Department of Medicine, Stanford University, Stanford, CA 94305, USA. Department of Urology, Cleveland Clinic Foundation, Cleveland, OH 44195, USA. Howard Hughes Medical Institute (HHMI), Chevy Chase, MD 20815, USA. Duke University School of Medicine, Durham, NC 27710, USA. ; Department of Neurology, UCSF, San Francisco, CA 94158, USA. ; Department of Pediatrics, University of California at San Francisco (UCSF), San Francisco, CA 94158, USA. Department of Neurology, UCSF, San Francisco, CA 94158, USA. Division of Neonatology, UCSF, San Francisco, CA 94158, USA. Newborn Brain Research Institute, UCSF, San Francisco, CA 94158, USA. stephen.fancy@ucsf.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26798014" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Vessels/cytology/embryology ; *Cell Movement ; Cerebral Cortex/blood supply/*embryology ; Endothelium, Vascular/cytology ; Humans ; Mice ; Neural Stem Cells/cytology/*physiology ; *Neurogenesis ; Oligodendroglia/cytology/*physiology ; *Organogenesis ; Pericytes/cytology/physiology ; Receptors, CXCR4/metabolism ; Signal Transduction ; Spinal Cord/blood supply/cytology/*embryology ; Wnt Proteins/metabolism
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  • 35
    Publication Date: 2016-02-26
    Description: Astrocytes are specialized and heterogeneous cells that contribute to central nervous system function and homeostasis. However, the mechanisms that create and maintain differences among astrocytes and allow them to fulfill particular physiological roles remain poorly defined. We reveal that neurons actively determine the features of astrocytes in the healthy adult brain and define a role for neuron-derived sonic hedgehog (Shh) in regulating the molecular and functional profile of astrocytes. Thus, the molecular and physiological program of astrocytes is not hardwired during development but, rather, depends on cues from neurons that drive and sustain their specialized properties.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Farmer, W Todd -- Abrahamsson, Therese -- Chierzi, Sabrina -- Lui, Christopher -- Zaelzer, Cristian -- Jones, Emma V -- Bally, Blandine Ponroy -- Chen, Gary G -- Theroux, Jean-Francois -- Peng, Jimmy -- Bourque, Charles W -- Charron, Frederic -- Ernst, Carl -- Sjostrom, P Jesper -- Murai, Keith K -- FDN 143337/Canadian Institutes of Health Research/Canada -- MOP 111152/Canadian Institutes of Health Research/Canada -- MOP 123390/Canadian Institutes of Health Research/Canada -- MOP 126137/Canadian Institutes of Health Research/Canada -- NIA 288936/Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2016 Feb 19;351(6275):849-54. doi: 10.1126/science.aab3103.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Research in Neuroscience, Department of Neurology and Neurosurgery, Brain Repair and Integrative Neuroscience Program, The Research Institute of the McGill University Health Centre, Montreal General Hospital, Montreal, Quebec, Canada. ; Department of Psychiatry, McGill University, Montreal, Quebec, Canada. McGill Group for Suicide Studies, Douglas Hospital, Montreal, Quebec, Canada. ; Molecular Biology of Neural Development, Institut de Recherches Cliniques de Montreal, Department of Medicine, University of Montreal, Montreal, Quebec, Canada. Department of Biology, McGill University, Montreal, Quebec, Canada. ; Department of Psychiatry, McGill University, Montreal, Quebec, Canada. McGill Group for Suicide Studies, Douglas Hospital, Montreal, Quebec, Canada. Department of Human Genetics, McGill University, Montreal, Quebec, Canada. Douglas Hospital Research Institute, Verdun, Quebec, Canada. ; Centre for Research in Neuroscience, Department of Neurology and Neurosurgery, Brain Repair and Integrative Neuroscience Program, The Research Institute of the McGill University Health Centre, Montreal General Hospital, Montreal, Quebec, Canada. keith.murai@mcgill.ca.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912893" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/*metabolism ; Cerebellar Cortex/*cytology ; Female ; Gene Deletion ; Hedgehog Proteins/genetics/*metabolism ; Male ; Mice ; Mice, Mutant Strains ; Neurons/*metabolism ; Receptors, G-Protein-Coupled/genetics/*metabolism ; Signal Transduction
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  • 36
    Publication Date: 2016-02-26
    Description: Purine biosynthetic enzymes organize into dynamic cellular bodies called purinosomes. Little is known about the spatiotemporal control of these structures. Using super-resolution microscopy, we demonstrated that purinosomes colocalized with mitochondria, and these results were supported by isolation of purinosome enzymes with mitochondria. Moreover, the number of purinosome-containing cells responded to dysregulation of mitochondrial function and metabolism. To explore the role of intracellular signaling, we performed a kinome screen using a label-free assay and found that mechanistic target of rapamycin (mTOR) influenced purinosome assembly. mTOR inhibition reduced purinosome-mitochondria colocalization and suppressed purinosome formation stimulated by mitochondria dysregulation. Collectively, our data suggest an mTOR-mediated link between purinosomes and mitochondria, and a general means by which mTOR regulates nucleotide metabolism by spatiotemporal control over protein association.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉French, Jarrod B -- Jones, Sara A -- Deng, Huayun -- Pedley, Anthony M -- Kim, Doory -- Chan, Chung Yu -- Hu, Haibei -- Pugh, Raymond J -- Zhao, Hong -- Zhang, Youxin -- Huang, Tony Jun -- Fang, Ye -- Zhuang, Xiaowei -- Benkovic, Stephen J -- 1R33EB019785-01/EB/NIBIB NIH HHS/ -- GM024129/GM/NIGMS NIH HHS/ -- Canadian Institutes of Health Research/Canada -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2016 Feb 12;351(6274):733-7. doi: 10.1126/science.aac6054.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Cell Biology, Department of Chemistry, Stony Brook University, Stony Brook, NY 11794, USA. jarrod.french@stonybrook.edu fangy2@corning.com zhuang@chemistry.harvard.edu sjb1@psu.edu. ; Department of Chemistry and Chemical Biology, Harvard University, Cambridge, MA 02138, USA. ; Biochemical Technologies, Science and Technology Division, Corning Incorporated, Corning, NY 14831, USA. ; Department of Chemistry, The Pennsylvania State University, University Park, PA 16802, USA. ; Department of Chemistry and Chemical Biology, Harvard University, Cambridge, MA 02138, USA. Howard Hughes Medical Institute, Harvard University, Cambridge, MA 02138, USA. ; Department of Engineering Science and Mechanics, The Pennsylvania State University, University Park, PA 16802, USA. ; Biochemical Technologies, Science and Technology Division, Corning Incorporated, Corning, NY 14831, USA. jarrod.french@stonybrook.edu fangy2@corning.com zhuang@chemistry.harvard.edu sjb1@psu.edu. ; Department of Chemistry and Chemical Biology, Harvard University, Cambridge, MA 02138, USA. Howard Hughes Medical Institute, Harvard University, Cambridge, MA 02138, USA. Department of Physics, Harvard University, Cambridge, MA 02138, USA. jarrod.french@stonybrook.edu fangy2@corning.com zhuang@chemistry.harvard.edu sjb1@psu.edu. ; Department of Chemistry, The Pennsylvania State University, University Park, PA 16802, USA. jarrod.french@stonybrook.edu fangy2@corning.com zhuang@chemistry.harvard.edu sjb1@psu.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912862" target="_blank"〉PubMed〈/a〉
    Keywords: HeLa Cells ; Humans ; Microscopy ; Mitochondria/*metabolism/ultrastructure ; Purines/*metabolism ; Signal Transduction ; TOR Serine-Threonine Kinases/*metabolism
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  • 37
    Publication Date: 2016-02-26
    Description: Bruns and Taylor argue that our finding of widespread distribution among Glomeromycota "virtual taxa" is undermined by the species definition applied. Although identifying appropriate species concepts and accessing taxonomically informative traits are challenges for microorganism biogeography, the virtual taxa represent a pragmatic classification that corresponds approximately to the species rank of classical Glomeromycota taxonomy, yet is applicable to environmental DNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Opik, Maarja -- Davison, John -- Moora, Mari -- Partel, Meelis -- Zobel, Martin -- New York, N.Y. -- Science. 2016 Feb 19;351(6275):826. doi: 10.1126/science.aad5495.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Botany, University of Tartu, 40 Lai Street, 51005 Tartu, Estonia. maarja.opik@ut.ee. ; Department of Botany, University of Tartu, 40 Lai Street, 51005 Tartu, Estonia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912890" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Ecosystem ; Humans ; *Mycorrhizae ; Plant Roots/*microbiology ; *Symbiosis
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  • 38
    Publication Date: 2016-01-23
    Description: The plant root cap, surrounding the very tip of the growing root, perceives and transmits environmental signals to the inner root tissues. In Arabidopsis thaliana, auxin released by the root cap contributes to the regular spacing of lateral organs along the primary root axis. Here, we show that the periodicity of lateral organ induction is driven by recurrent programmed cell death at the most distal edge of the root cap. We suggest that synchronous bursts of cell death in lateral root cap cells release pulses of auxin to surrounding root tissues, establishing the pattern for lateral root formation. The dynamics of root cap turnover may therefore coordinate primary root growth with root branching in order to optimize the uptake of water and nutrients from the soil.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xuan, Wei -- Band, Leah R -- Kumpf, Robert P -- Van Damme, Daniel -- Parizot, Boris -- De Rop, Gieljan -- Opdenacker, Davy -- Moller, Barbara K -- Skorzinski, Noemi -- Njo, Maria F -- De Rybel, Bert -- Audenaert, Dominique -- Nowack, Moritz K -- Vanneste, Steffen -- Beeckman, Tom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- New York, N.Y. -- Science. 2016 Jan 22;351(6271):384-7. doi: 10.1126/science.aad2776.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Plant Systems Biology, Vlaams Instituut voor Biotechnologie (VIB), Technologiepark 927, 9052 Ghent, Belgium. Department of Plant Biotechnology and Bioinformatics, Gent University, Technologiepark 927, 9052 Ghent, Belgium. State Key Laboratory of Crop Genetics and Germplasm Enhancement and MOA Key Laboratory of Plant Nutrition and Fertilization in Lower-Middle Reaches of the Yangtze River, Nanjing Agricultural University, Weigang No. 1, Nanjing 210095, PR China. ; Centre for Plant Integrative Biology, University of Nottingham, Nottingham LE12 5RD, UK. ; Department of Plant Systems Biology, Vlaams Instituut voor Biotechnologie (VIB), Technologiepark 927, 9052 Ghent, Belgium. Department of Plant Biotechnology and Bioinformatics, Gent University, Technologiepark 927, 9052 Ghent, Belgium. ; Max Planck Institute for Developmental Biology, Spemannstrasse 35, 72076 Tubingen, Germany. ; Department of Plant Systems Biology, Vlaams Instituut voor Biotechnologie (VIB), Technologiepark 927, 9052 Ghent, Belgium. Department of Plant Biotechnology and Bioinformatics, Gent University, Technologiepark 927, 9052 Ghent, Belgium. Laboratory of Biochemistry, Wageningen University, Dreijenlaan 3, 6703HA Wageningen, Netherlands. ; Department of Plant Systems Biology, Vlaams Instituut voor Biotechnologie (VIB), Technologiepark 927, 9052 Ghent, Belgium. Department of Plant Biotechnology and Bioinformatics, Gent University, Technologiepark 927, 9052 Ghent, Belgium. tobee@psb.vib-ugent.be.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26798015" target="_blank"〉PubMed〈/a〉
    Keywords: *Apoptosis ; Arabidopsis/cytology/*growth & development/metabolism ; Indoleacetic Acids/*metabolism ; Plant Epidermis/cytology/growth & development/metabolism ; Plant Root Cap/cytology/*growth & development/metabolism ; Receptors, TNF-Related Apoptosis-Inducing Ligand/genetics/metabolism ; Signal Transduction ; Soil ; Water/metabolism
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  • 39
    Publication Date: 2016-02-06
    Description: The intestinal epithelium forms an essential barrier between a host and its microbiota. Protozoa and helminths are members of the gut microbiota of mammals, including humans, yet the many ways that gut epithelial cells orchestrate responses to these eukaryotes remain unclear. Here we show that tuft cells, which are taste-chemosensory epithelial cells, accumulate during parasite colonization and infection. Disruption of chemosensory signaling through the loss of TRMP5 abrogates the expansion of tuft cells, goblet cells, eosinophils, and type 2 innate lymphoid cells during parasite colonization. Tuft cells are the primary source of the parasite-induced cytokine interleukin-25, which indirectly induces tuft cell expansion by promoting interleukin-13 production by innate lymphoid cells. Our results identify intestinal tuft cells as critical sentinels in the gut epithelium that promote type 2 immunity in response to intestinal parasites.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Howitt, Michael R -- Lavoie, Sydney -- Michaud, Monia -- Blum, Arthur M -- Tran, Sara V -- Weinstock, Joel V -- Gallini, Carey Ann -- Redding, Kevin -- Margolskee, Robert F -- Osborne, Lisa C -- Artis, David -- Garrett, Wendy S -- F31DK105653/DK/NIDDK NIH HHS/ -- F32DK098826/DK/NIDDK NIH HHS/ -- R01 CA154426/CA/NCI NIH HHS/ -- R01 GM099531/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2016 Mar 18;351(6279):1329-33. doi: 10.1126/science.aaf1648. Epub 2016 Feb 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Immunology and Infectious Diseases and Genetics and Complex Diseases, Harvard T. H. Chan School of Public Health, Boston, MA 02115, USA. ; Division of Gastroenterology, Tufts Medical Center, Boston, MA 02111, USA. ; Monell Chemical Senses Center, Philadelphia, PA 19104, USA. ; Jill Roberts Institute for Research in Inflammatory Bowel Disease, Weill Cornell Medical College, Cornell University, New York, NY 10021, USA. ; Departments of Immunology and Infectious Diseases and Genetics and Complex Diseases, Harvard T. H. Chan School of Public Health, Boston, MA 02115, USA. Broad Institute of Harvard and Massachusetts Institute of Technology, Cambridge, MA 02142, USA. Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA. wgarrett@hsph.harvard.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26847546" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chemoreceptor Cells/*immunology ; Eosinophils/immunology ; Goblet Cells/immunology ; Helminthiasis/immunology/parasitology ; Helminths/immunology ; Immunity, Mucosal ; Interleukin-13/immunology ; Interleukin-17/immunology ; Intestinal Diseases, Parasitic/*immunology/parasitology ; Intestinal Mucosa/*immunology/*parasitology ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Microbiota/*immunology ; Protein-Serine-Threonine Kinases/immunology ; Protozoan Infections/immunology/parasitology ; Signal Transduction ; TRPM Cation Channels/*immunology ; Taste ; Transducin/genetics/immunology ; Tritrichomonas/immunology
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  • 40
    Publication Date: 2016-02-06
    Description: SH3 and multiple ankyrin repeat domains 3 (SHANK3) haploinsufficiency is causative for the neurological features of Phelan-McDermid syndrome (PMDS), including a high risk of autism spectrum disorder (ASD). We used unbiased, quantitative proteomics to identify changes in the phosphoproteome of Shank3-deficient neurons. Down-regulation of protein kinase B (PKB/Akt)-mammalian target of rapamycin complex 1 (mTORC1) signaling resulted from enhanced phosphorylation and activation of serine/threonine protein phosphatase 2A (PP2A) regulatory subunit, B56beta, due to increased steady-state levels of its kinase, Cdc2-like kinase 2 (CLK2). Pharmacological and genetic activation of Akt or inhibition of CLK2 relieved synaptic deficits in Shank3-deficient and PMDS patient-derived neurons. CLK2 inhibition also restored normal sociability in a Shank3-deficient mouse model. Our study thereby provides a novel mechanistic and potentially therapeutic understanding of deregulated signaling downstream of Shank3 deficiency.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bidinosti, Michael -- Botta, Paolo -- Kruttner, Sebastian -- Proenca, Catia C -- Stoehr, Natacha -- Bernhard, Mario -- Fruh, Isabelle -- Mueller, Matthias -- Bonenfant, Debora -- Voshol, Hans -- Carbone, Walter -- Neal, Sarah J -- McTighe, Stephanie M -- Roma, Guglielmo -- Dolmetsch, Ricardo E -- Porter, Jeffrey A -- Caroni, Pico -- Bouwmeester, Tewis -- Luthi, Andreas -- Galimberti, Ivan -- New York, N.Y. -- Science. 2016 Mar 11;351(6278):1199-203. doi: 10.1126/science.aad5487. Epub 2016 Feb 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Developmental Molecular Pathways, Novartis Institutes for Biomedical Research, Basel, Switzerland. ; Friedrich Miescher Institute, Basel, Switzerland. ; Analytical Sciences and Imaging, Novartis Institutes for Biomedical Research, Basel, Switzerland. ; Neuroscience, Novartis Institutes for Biomedical Research, Cambridge, USA. ; Developmental Molecular Pathways, Novartis Institutes for Biomedical Research, Basel, Switzerland. ivan.galimberti@novartis.com.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26847545" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Autism Spectrum Disorder/*drug therapy/enzymology/genetics ; Chromosome Deletion ; Chromosome Disorders/genetics ; Chromosomes, Human, Pair 22/genetics ; Disease Models, Animal ; Down-Regulation ; Gene Knockdown Techniques ; Humans ; Insulin-Like Growth Factor I/metabolism ; Mice ; Molecular Sequence Data ; Multiprotein Complexes/metabolism ; Nerve Tissue Proteins/*genetics ; Neurons/enzymology ; Phosphorylation ; Protein Phosphatase 2/metabolism ; Protein-Serine-Threonine Kinases/*antagonists & inhibitors/metabolism ; Protein-Tyrosine Kinases/*antagonists & inhibitors/metabolism ; Proteomics ; Proto-Oncogene Proteins c-akt/genetics/metabolism ; Rats ; Signal Transduction ; TOR Serine-Threonine Kinases/metabolism
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  • 41
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-29
    Description: Metastatic disease is the leading cause of cancer-related deaths and involves critical interactions between tumor cells and the microenvironment. Hypoxia is a potent microenvironmental factor promoting metastatic progression. Clinically, hypoxia and the expression of the hypoxia-inducible transcription factors HIF-1 and HIF-2 are associated with increased distant metastasis and poor survival in a variety of tumor types. Moreover, HIF signaling in malignant cells influences multiple steps within the metastatic cascade. Here we review research focused on elucidating the mechanisms by which the hypoxic tumor microenvironment promotes metastatic progression. These studies have identified potential biomarkers and therapeutic targets regulated by hypoxia that could be incorporated into strategies aimed at preventing and treating metastatic disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rankin, Erinn B -- Giaccia, Amato J -- CA-197713/CA/NCI NIH HHS/ -- CA-198291/CA/NCI NIH HHS/ -- CA-67166/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2016 Apr 8;352(6282):175-80. doi: 10.1126/science.aaf4405. Epub 2016 Apr 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University Medical Center, Stanford, CA 94305-5152, USA. Department of Obstetrics and Gynecology, Stanford University Medical Center, Stanford, CA 94305-5152, USA. ; Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University Medical Center, Stanford, CA 94305-5152, USA. giaccia@stanford.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27124451" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic Helix-Loop-Helix Transcription Factors/*metabolism ; Biomarkers, Tumor/analysis/metabolism ; Cell Hypoxia ; Cell Movement ; Disease Progression ; Drug Resistance, Neoplasm ; Epithelial-Mesenchymal Transition ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/*metabolism ; Neoplasm Invasiveness ; Neoplasm Metastasis/*pathology/*therapy ; Radiation Tolerance ; Signal Transduction ; *Tumor Microenvironment
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  • 42
    Publication Date: 2016-02-26
    Description: Davison et al. (Reports, 28 August 2015, p. 970) claim that virtual taxa of Glomeromycota show little endemism and that endemism that exists is similar to the levels seen in plant families. We show that this is likely due to the conservative species definition rather than to any ecological pattern.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bruns, Thomas D -- Taylor, John W -- New York, N.Y. -- Science. 2016 Feb 19;351(6275):826. doi: 10.1126/science.aad4228.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Plant and Microbial Biology, 111 Koshland Hall, Berkeley, CA 94720-3102, USA. pogon@berkeley.edu. ; Department of Plant and Microbial Biology, 111 Koshland Hall, Berkeley, CA 94720-3102, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912889" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Ecosystem ; Humans ; *Mycorrhizae ; Plant Roots/*microbiology ; *Symbiosis
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  • 43
    Publication Date: 2016-03-12
    Description: The oncogene MDMX is overexpressed in many cancers, leading to suppression of the tumor suppressor p53. Inhibitors of the oncogene product MDMX therefore might help reactivate p53 and enhance the efficacy of DNA-damaging drugs. However, we currently lack a quantitative understanding of how MDMX inhibition affects the p53 signaling pathway and cell sensitivity to DNA damage. Live cell imaging showed that MDMX depletion triggered two distinct phases of p53 accumulation in single cells: an initial postmitotic pulse, followed by low-amplitude oscillations. The response to DNA damage was sharply different in these two phases; in the first phase, MDMX depletion was synergistic with DNA damage in causing cell death, whereas in the second phase, depletion of MDMX inhibited cell death. Thus a quantitative understanding of signal dynamics and cellular states is important for designing an optimal schedule of dual-drug administration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Sheng-Hong -- Forrester, William -- Lahav, Galit -- F32GM105205/GM/NIGMS NIH HHS/ -- GM083303/GM/NIGMS NIH HHS/ -- R01 GM083303/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2016 Mar 11;351(6278):1204-8. doi: 10.1126/science.aac5610. Epub 2016 Mar 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Systems Biology, Harvard Medical School, Boston, MA, USA. ; Developmental and Molecular Pathways, Novartis Institutes for Biomedical Research, Cambridge, MA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26965628" target="_blank"〉PubMed〈/a〉
    Keywords: Antineoplastic Agents/*administration & dosage ; Apoptosis ; *DNA Damage ; Gene Knockdown Techniques ; Humans ; MCF-7 Cells ; Molecular Imaging ; Neoplasms/*drug therapy ; Proto-Oncogene Proteins c-mdm2/*antagonists & inhibitors/genetics ; RNA, Small Interfering/genetics ; Signal Transduction ; Time Factors ; Tumor Suppressor Protein p53/*metabolism
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  • 44
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2016-11-18
    Description: Author: Jake Yeston
    Keywords: Organic Chemistry
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  • 45
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2016-11-18
    Description: Author: Jake Yeston
    Keywords: Organic Chemistry
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  • 46
    Publication Date: 2016-02-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huete, Alfredo -- England -- Nature. 2016 Mar 10;531(7593):181-2. doi: 10.1038/nature17301. Epub 2016 Feb 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Plant Functional Biology and Climate Change Cluster, University of Technology Sydney, Ultimo, New South Wales 2007, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26886792" target="_blank"〉PubMed〈/a〉
    Keywords: *Acclimatization ; *Climate Change ; *Ecosystem ; *Geographic Mapping ; *Plant Physiological Phenomena
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  • 47
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    Unknown
    Nature Publishing Group (NPG)
    Publication Date: 2016-04-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Caron, David A -- England -- Nature. 2016 Apr 28;532(7600):444-5. doi: 10.1038/nature17892. Epub 2016 Apr 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, University of Southern California, Los Angeles, California 90089-0371, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27096370" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aquatic Organisms/*metabolism ; *Biomass ; *Biota ; Carbon/*metabolism ; *Ecosystem ; *Oceans and Seas ; Plankton/*metabolism ; Rhizaria/*isolation & purification ; Seawater/*chemistry ; Zooplankton/*isolation & purification
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  • 48
    Publication Date: 2016-01-07
    Description: Endothelial cells (ECs) are plastic cells that can switch between growth states with different bioenergetic and biosynthetic requirements. Although quiescent in most healthy tissues, ECs divide and migrate rapidly upon proangiogenic stimulation. Adjusting endothelial metabolism to the growth state is central to normal vessel growth and function, yet it is poorly understood at the molecular level. Here we report that the forkhead box O (FOXO) transcription factor FOXO1 is an essential regulator of vascular growth that couples metabolic and proliferative activities in ECs. Endothelial-restricted deletion of FOXO1 in mice induces a profound increase in EC proliferation that interferes with coordinated sprouting, thereby causing hyperplasia and vessel enlargement. Conversely, forced expression of FOXO1 restricts vascular expansion and leads to vessel thinning and hypobranching. We find that FOXO1 acts as a gatekeeper of endothelial quiescence, which decelerates metabolic activity by reducing glycolysis and mitochondrial respiration. Mechanistically, FOXO1 suppresses signalling by MYC (also known as c-MYC), a powerful driver of anabolic metabolism and growth. MYC ablation impairs glycolysis, mitochondrial function and proliferation of ECs while its EC-specific overexpression fuels these processes. Moreover, restoration of MYC signalling in FOXO1-overexpressing endothelium normalizes metabolic activity and branching behaviour. Our findings identify FOXO1 as a critical rheostat of vascular expansion and define the FOXO1-MYC transcriptional network as a novel metabolic checkpoint during endothelial growth and proliferation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilhelm, Kerstin -- Happel, Katharina -- Eelen, Guy -- Schoors, Sandra -- Oellerich, Mark F -- Lim, Radiance -- Zimmermann, Barbara -- Aspalter, Irene M -- Franco, Claudio A -- Boettger, Thomas -- Braun, Thomas -- Fruttiger, Marcus -- Rajewsky, Klaus -- Keller, Charles -- Bruning, Jens C -- Gerhardt, Holger -- Carmeliet, Peter -- Potente, Michael -- K08CA090438/CA/NCI NIH HHS/ -- Cancer Research UK/United Kingdom -- England -- Nature. 2016 Jan 14;529(7585):216-20. doi: 10.1038/nature16498. Epub 2016 Jan 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Angiogenesis &Metabolism Laboratory, Max Planck Institute for Heart and Lung Research, D-61231 Bad Nauheim, Germany. ; Laboratory of Angiogenesis and Neurovascular Link, Vesalius Research Center, Department of Oncology, University of Leuven, Leuven 3000, Belgium. ; Laboratory of Angiogenesis and Neurovascular Link, Vesalius Research Center, VIB, Leuven 3000, Belgium. ; Vascular Biology Laboratory, London Research Institute, Cancer Research UK, London WC2A 3LY, UK. ; Vascular Morphogenesis Laboratory, Instituto de Medicina Molecular, Faculdade de Medicina da Universidade de Lisboa, Lisbon 1649-028, Portugal. ; Department of Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, D-61231 Bad Nauheim, Germany. ; UCL Institute of Ophthalmology, University College London, London EC1V 9EL, UK. ; Max Delbruck Center for Molecular Medicine (MDC), D-13125 Berlin, Germany. ; Children's Cancer Therapy Development Institute, Beaverton, Oregon 97005, USA. ; Max Planck Institute for Metabolism Research, Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD) and Center of Molecular Medicine Cologne (CMMC), Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University of Cologne, D-50931 Cologne, Germany. ; Vascular Patterning Laboratory, Vesalius Research Center, VIB and University of Leuven, Leuven 3000, Belgium. ; DZHK (German Center for Cardiovascular Research), partner site Berlin, D-13347 Berlin, Germany. ; Berlin Institute of Health (BIH), D-10117 Berlin, Germany. ; International Institute of Molecular and Cell Biology, 02-109 Warsaw, Poland. ; DZHK (German Center for Cardiovascular Research), partner site Frankfurt Rhine-Main, D-13347 Berlin, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26735015" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Proliferation ; Cell Respiration ; Endothelium, Vascular/cytology/*growth & development/*metabolism ; Female ; Forkhead Transcription Factors/deficiency/genetics/*metabolism ; Glycolysis ; Human Umbilical Vein Endothelial Cells/cytology/metabolism ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Proto-Oncogene Proteins c-myc/deficiency/genetics/metabolism ; Signal Transduction
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  • 49
    Publication Date: 2016-05-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Jihong -- Liu, Xiang -- England -- Nature. 2016 May 18;533(7603):321. doi: 10.1038/533321d.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Shanghai Maritime University, China. ; Rutgers University, Piscataway, New Jersey, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27193671" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Dissent and Disputes ; *Ecosystem ; *Environmental Monitoring ; *Models, Economic ; *Transportation
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  • 50
    Publication Date: 2016-03-11
    Description: The terrestrial biosphere can release or absorb the greenhouse gases, carbon dioxide (CO2), methane (CH4) and nitrous oxide (N2O), and therefore has an important role in regulating atmospheric composition and climate. Anthropogenic activities such as land-use change, agriculture and waste management have altered terrestrial biogenic greenhouse gas fluxes, and the resulting increases in methane and nitrous oxide emissions in particular can contribute to climate change. The terrestrial biogenic fluxes of individual greenhouse gases have been studied extensively, but the net biogenic greenhouse gas balance resulting from anthropogenic activities and its effect on the climate system remains uncertain. Here we use bottom-up (inventory, statistical extrapolation of local flux measurements, and process-based modelling) and top-down (atmospheric inversions) approaches to quantify the global net biogenic greenhouse gas balance between 1981 and 2010 resulting from anthropogenic activities and its effect on the climate system. We find that the cumulative warming capacity of concurrent biogenic methane and nitrous oxide emissions is a factor of about two larger than the cooling effect resulting from the global land carbon dioxide uptake from 2001 to 2010. This results in a net positive cumulative impact of the three greenhouse gases on the planetary energy budget, with a best estimate (in petagrams of CO2 equivalent per year) of 3.9 +/- 3.8 (top down) and 5.4 +/- 4.8 (bottom up) based on the GWP100 metric (global warming potential on a 100-year time horizon). Our findings suggest that a reduction in agricultural methane and nitrous oxide emissions, particularly in Southern Asia, may help mitigate climate change.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tian, Hanqin -- Lu, Chaoqun -- Ciais, Philippe -- Michalak, Anna M -- Canadell, Josep G -- Saikawa, Eri -- Huntzinger, Deborah N -- Gurney, Kevin R -- Sitch, Stephen -- Zhang, Bowen -- Yang, Jia -- Bousquet, Philippe -- Bruhwiler, Lori -- Chen, Guangsheng -- Dlugokencky, Edward -- Friedlingstein, Pierre -- Melillo, Jerry -- Pan, Shufen -- Poulter, Benjamin -- Prinn, Ronald -- Saunois, Marielle -- Schwalm, Christopher R -- Wofsy, Steven C -- England -- Nature. 2016 Mar 10;531(7593):225-8. doi: 10.1038/nature16946.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉International Center for Climate and Global Change Research, School of Forestry and Wildlife Sciences, Auburn University, Auburn, Alabama 36849, USA. ; Department of Ecology, Evolution, and Organismal Biology, Iowa State University, Iowa 50011, USA. ; Laboratoire des Sciences du Climat et de l'Environnement, 91191 Gif sur Yvette, France. ; Department of Global Ecology, Carnegie Institution for Science, Stanford, California 94305, USA. ; Global Carbon Project, CSIRO Oceans and Atmosphere Research, GPO Box 3023, Canberra, Australian Capital Territory 2601, Australia. ; Department of Environmental Sciences, Emory University, Atlanta, Georgia 30322, USA. ; School of Earth Sciences and Environmental Sustainability, Northern Arizona University, Flagstaff, Arizona 86011, USA. ; School of Life Sciences, Arizona State University, Tempe, Arizona 85287, USA. ; College of Life and Environmental Sciences, University of Exeter, Exeter EX4 4RJ, UK. ; NOAA Earth System Research Laboratory, Global Monitoring Division, Boulder, Colorado 80305, USA. ; Environmental Science Division, Oak Ridge National Laboratory, Oak Ridge, Tennessee 37831, USA. ; College of Engineering, Mathematics and Physical Sciences, University of Exeter, Exeter EX4 4QF, UK. ; The Ecosystems Center, Marine Biological Laboratory, Woods Hole, Massachusetts 02543, USA. ; Institute of Ecosystems and Department of Ecology, Montana State University, Bozeman, Montana 59717, USA. ; Center for Global Change Science, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA. ; Woods Hole Research Center, Falmouth, Massachusetts 02540, USA. ; Department of Earth and Planetary Science, Harvard University, 29 Oxford Street, Cambridge, Massachusetts 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26961656" target="_blank"〉PubMed〈/a〉
    Keywords: Agriculture/statistics & numerical data ; Asia ; Atmosphere/*chemistry ; Carbon Dioxide/analysis/*metabolism ; *Ecosystem ; Global Warming/prevention & control/*statistics & numerical data ; Greenhouse Effect/prevention & control/*statistics & numerical data ; Human Activities/statistics & numerical data ; Methane/analysis/*metabolism ; Nitrous Oxide/analysis/*metabolism
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  • 51
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    Nature Publishing Group (NPG)
    Publication Date: 2016-05-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mehrabi, Zia -- England -- Nature. 2016 May 25;533(7604):469. doi: 10.1038/533469c.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of British Columbia, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27225111" target="_blank"〉PubMed〈/a〉
    Keywords: Conservation of Natural Resources/*methods ; *Ecosystem ; *Wilderness
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  • 52
    Publication Date: 2016-02-11
    Description: The biological carbon pump is the process by which CO2 is transformed to organic carbon via photosynthesis, exported through sinking particles, and finally sequestered in the deep ocean. While the intensity of the pump correlates with plankton community composition, the underlying ecosystem structure driving the process remains largely uncharacterized. Here we use environmental and metagenomic data gathered during the Tara Oceans expedition to improve our understanding of carbon export in the oligotrophic ocean. We show that specific plankton communities, from the surface and deep chlorophyll maximum, correlate with carbon export at 150 m and highlight unexpected taxa such as Radiolaria and alveolate parasites, as well as Synechococcus and their phages, as lineages most strongly associated with carbon export in the subtropical, nutrient-depleted, oligotrophic ocean. Additionally, we show that the relative abundance of a few bacterial and viral genes can predict a significant fraction of the variability in carbon export in these regions.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4851848/" 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/PMC4851848/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guidi, Lionel -- Chaffron, Samuel -- Bittner, Lucie -- Eveillard, Damien -- Larhlimi, Abdelhalim -- Roux, Simon -- Darzi, Youssef -- Audic, Stephane -- Berline, Leo -- Brum, Jennifer R -- Coelho, Luis Pedro -- Espinoza, Julio Cesar Ignacio -- Malviya, Shruti -- Sunagawa, Shinichi -- Dimier, Celine -- Kandels-Lewis, Stefanie -- Picheral, Marc -- Poulain, Julie -- Searson, Sarah -- Tara Oceans Consortium Coordinators -- Stemmann, Lars -- Not, Fabrice -- Hingamp, Pascal -- Speich, Sabrina -- Follows, Mick -- Karp-Boss, Lee -- Boss, Emmanuel -- Ogata, Hiroyuki -- Pesant, Stephane -- Weissenbach, Jean -- Wincker, Patrick -- Acinas, Silvia G -- Bork, Peer -- de Vargas, Colomban -- Iudicone, Daniele -- Sullivan, Matthew B -- Raes, Jeroen -- Karsenti, Eric -- Bowler, Chris -- Gorsky, Gabriel -- England -- Nature. 2016 Apr 28;532(7600):465-70. doi: 10.1038/nature16942. Epub 2016 Feb 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sorbonne Universites, UPMC Universite Paris 06, CNRS, Laboratoire d'oceanographie de Villefranche (LOV), Observatoire Oceanologique, 06230 Villefranche-sur-Mer, France. ; Department of Oceanography, University of Hawaii, Honolulu, Hawaii 96822, USA. ; Department of Microbiology and Immunology, Rega Institute, KU Leuven, Herestraat 49, 3000 Leuven, Belgium. ; Center for the Biology of Disease, VIB, Herestraat 49, 3000 Leuven, Belgium. ; Department of Applied Biological Sciences, Vrije Universiteit Brussel, Pleinlaan 2, 1050 Brussels, Belgium. ; Sorbonne Universites, UPMC Univ Paris 06, CNRS, Institut de Biologie Paris-Seine (IBPS), Evolution Paris Seine, F-75005, Paris, France. ; Ecole Normale Superieure, PSL Research University, Institut de Biologie de l'Ecole Normale Superieure (IBENS), CNRS UMR 8197, INSERM U1024, 46 rue d'Ulm, F-75005 Paris, France. ; Sorbonne Universites, UPMC Universite Paris 06, CNRS, Laboratoire Adaptation et Diversite en Milieu Marin, Station Biologique de Roscoff, 29680 Roscoff, France. ; LINA UMR 6241, Universite de Nantes, EMN, CNRS, 44322 Nantes, France. ; Department of Ecology and Evolutionary Biology, University of Arizona, Tucson, Arizona 85721, USA. ; Structural and Computational Biology, European Molecular Biology Laboratory, Meyerhofstr. 1, 69117 Heidelberg, Germany. ; Directors' Research European Molecular Biology Laboratory Meyerhofstr. 1, 69117 Heidelberg, Germany. ; CEA - Institut de Genomique, GENOSCOPE, 2 rue Gaston Cremieux, 91057 Evry, France. ; Aix Marseille Universite, CNRS, IGS, UMR 7256, 13288 Marseille, France. ; Department of Geosciences, Laboratoire de Meteorologie Dynamique (LMD), Ecole Normale Superieure, 24 rue Lhomond, 75231 Paris CEDEX 05, France. ; Dept of Earth, Atmospheric and Planetary Sciences, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA. ; School of Marine Sciences, University of Maine, Orono, Maine 04469, USA. ; Institute for Chemical Research, Kyoto University, Gokasho, Uji, Kyoto, 611-0011, Japan. ; PANGAEA, Data Publisher for Earth and Environmental Science, University of Bremen, 28359 Bremen, Germany. ; MARUM, Center for Marine Environmental Sciences, University of Bremen, 28359 Bremen, Germany. ; CNRS, UMR 8030, CP 5706 Evry, France. ; Universite d'Evry, UMR 8030, CP 5706 Evry, France. ; Department of Marine Biology and Oceanography, Institute of Marine Sciences (ICM)-CSIC, Pg. Maritim de la Barceloneta 37-49, Barcelona E0800, Spain. ; Max-Delbruck-Centre for Molecular Medicine, 13092 Berlin, Germany. ; Stazione Zoologica Anton Dohrn, Villa Comunale, 80121 Naples, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26863193" target="_blank"〉PubMed〈/a〉
    Keywords: Aquatic Organisms/genetics/isolation & purification/*metabolism ; Carbon/*metabolism ; Chlorophyll/metabolism ; Dinoflagellida/genetics/isolation & purification/metabolism ; *Ecosystem ; Expeditions ; Genes, Bacterial ; Genes, Viral ; Geography ; Oceans and Seas ; Photosynthesis ; Plankton/genetics/isolation & purification/*metabolism ; Seawater/*chemistry/microbiology/parasitology ; Synechococcus/genetics/isolation & purification/metabolism/virology
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  • 53
    Publication Date: 2016-05-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Breed, Martin F -- Lowe, Andrew J -- Mortimer, Peter E -- England -- Nature. 2016 May 25;533(7604):469. doi: 10.1038/533469d.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Adelaide, Australia. ; Kunming Institute of Botany; and World Agroforestry Centre, Kunming, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27225110" target="_blank"〉PubMed〈/a〉
    Keywords: Conservation of Natural Resources/*methods ; *Ecosystem ; *Wilderness
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  • 54
    Publication Date: 2016-03-17
    Description: Plant respiration results in an annual flux of carbon dioxide (CO2) to the atmosphere that is six times as large as that due to the emissions from fossil fuel burning, so changes in either will impact future climate. As plant respiration responds positively to temperature, a warming world may result in additional respiratory CO2 release, and hence further atmospheric warming. Plant respiration can acclimate to altered temperatures, however, weakening the positive feedback of plant respiration to rising global air temperature, but a lack of evidence on long-term (weeks to years) acclimation to climate warming in field settings currently hinders realistic predictions of respiratory release of CO2 under future climatic conditions. Here we demonstrate strong acclimation of leaf respiration to both experimental warming and seasonal temperature variation for juveniles of ten North American tree species growing for several years in forest conditions. Plants grown and measured at 3.4 degrees C above ambient temperature increased leaf respiration by an average of 5% compared to plants grown and measured at ambient temperature; without acclimation, these increases would have been 23%. Thus, acclimation eliminated 80% of the expected increase in leaf respiration of non-acclimated plants. Acclimation of leaf respiration per degree temperature change was similar for experimental warming and seasonal temperature variation. Moreover, the observed increase in leaf respiration per degree increase in temperature was less than half as large as the average reported for previous studies, which were conducted largely over shorter time scales in laboratory settings. If such dampening effects of leaf thermal acclimation occur generally, the increase in respiration rates of terrestrial plants in response to climate warming may be less than predicted, and thus may not raise atmospheric CO2 concentrations as much as anticipated.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reich, Peter B -- Sendall, Kerrie M -- Stefanski, Artur -- Wei, Xiaorong -- Rich, Roy L -- Montgomery, Rebecca A -- England -- Nature. 2016 Mar 31;531(7596):633-6. doi: 10.1038/nature17142. Epub 2016 Mar 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Forest Resources, University of Minnesota, Minnesota 55108, USA. ; Hawkesbury Institute for the Environment, Western Sydney University, Penrith, New South Wales 2753, Australia. ; State Key Laboratory of Soil Erosion and Dryland Farming on the Loess Plateau, Northwest A&F University, Yangling 712100, China. ; Smithsonian Environmental Research Center, Edgewater, Maryland 20137, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26982730" target="_blank"〉PubMed〈/a〉
    Keywords: *Acclimatization ; Atmosphere ; Carbon Dioxide/metabolism ; Cell Respiration ; Darkness ; *Ecosystem ; Forests ; *Global Warming ; North America ; Photosynthesis ; Plant Leaves/metabolism ; Seasons ; *Temperature ; Time Factors ; Trees/classification/*metabolism
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  • 55
    Publication Date: 2016-04-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kotiaho, Janne S -- ten Brink, Ben -- Harris, Jim -- England -- Nature. 2016 Apr 7;532(7597):37. doi: 10.1038/532037c.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Jyvaskyla, Finland. ; PBL-Netherlands Environmental Assessment Agency, The Netherlands. ; Cranfield University, Bedfordshire, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27078561" target="_blank"〉PubMed〈/a〉
    Keywords: Biodiversity ; Conservation of Natural Resources/*methods ; *Ecosystem ; Human Activities ; Reference Standards ; *Wilderness
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  • 56
    Publication Date: 2016-03-24
    Description: (beta-)Arrestins are important regulators of G-protein-coupled receptors (GPCRs). They bind to active, phosphorylated GPCRs and thereby shut off 'classical' signalling to G proteins, trigger internalization of GPCRs via interaction with the clathrin machinery and mediate signalling via 'non-classical' pathways. In addition to two visual arrestins that bind to rod and cone photoreceptors (termed arrestin1 and arrestin4), there are only two (non-visual) beta-arrestin proteins (beta-arrestin1 and beta-arrestin2, also termed arrestin2 and arrestin3), which regulate hundreds of different (non-visual) GPCRs. Binding of these proteins to GPCRs usually requires the active form of the receptors plus their phosphorylation by G-protein-coupled receptor kinases (GRKs). The binding of receptors or their carboxy terminus as well as certain truncations induce active conformations of (beta-)arrestins that have recently been solved by X-ray crystallography. Here we investigate both the interaction of beta-arrestin with GPCRs, and the beta-arrestin conformational changes in real time and in living human cells, using a series of fluorescence resonance energy transfer (FRET)-based beta-arrestin2 biosensors. We observe receptor-specific patterns of conformational changes in beta-arrestin2 that occur rapidly after the receptor-beta-arrestin2 interaction. After agonist removal, these changes persist for longer than the direct receptor interaction. Our data indicate a rapid, receptor-type-specific, two-step binding and activation process between GPCRs and beta-arrestins. They further indicate that beta-arrestins remain active after dissociation from receptors, allowing them to remain at the cell surface and presumably signal independently. Thus, GPCRs trigger a rapid, receptor-specific activation/deactivation cycle of beta-arrestins, which permits their active signalling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nuber, Susanne -- Zabel, Ulrike -- Lorenz, Kristina -- Nuber, Andreas -- Milligan, Graeme -- Tobin, Andrew B -- Lohse, Martin J -- Hoffmann, Carsten -- 1 R01 DA038882/DA/NIDA NIH HHS/ -- BB/K019864/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- England -- Nature. 2016 Mar 31;531(7596):661-4. doi: 10.1038/nature17198. Epub 2016 Mar 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Pharmacology and Toxicology, University of Wurzburg, Versbacher Str. 9, 97078 Wurzburg, Germany. ; Rudolf Virchow Center, University of Wurzburg, Versbacher Str. 9, 97078 Wurzburg, Germany. ; Comprehensive Heart Failure Center, University of Wurzburg, Versbacher Str. 9, 97078 Wurzburg, Germany. ; Molecular Pharmacology Group, Institute of Molecular, Cell and Systems Biology, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow G12 8QQ, UK. ; MRC Toxicology Unit, University of Leicester, Hodgkin Building, Lancaster Road, Leicester LE1 9HN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27007855" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arrestins/chemistry/*metabolism ; Biosensing Techniques ; Cattle ; Cell Line ; Cell Membrane/metabolism ; Cell Survival ; Crystallography, X-Ray ; Fluorescence Resonance Energy Transfer ; Humans ; Kinetics ; Models, Molecular ; Protein Binding ; Protein Conformation ; Receptors, G-Protein-Coupled/chemistry/*metabolism ; Signal Transduction ; Substrate Specificity ; Time Factors
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  • 57
    Publication Date: 2016-02-18
    Description: The identification of properties that contribute to the persistence and resilience of ecosystems despite climate change constitutes a research priority of global relevance. Here we present a novel, empirical approach to assess the relative sensitivity of ecosystems to climate variability, one property of resilience that builds on theoretical modelling work recognizing that systems closer to critical thresholds respond more sensitively to external perturbations. We develop a new metric, the vegetation sensitivity index, that identifies areas sensitive to climate variability over the past 14 years. The metric uses time series data derived from the moderate-resolution imaging spectroradiometer (MODIS) enhanced vegetation index, and three climatic variables that drive vegetation productivity (air temperature, water availability and cloud cover). Underlying the analysis is an autoregressive modelling approach used to identify climate drivers of vegetation productivity on monthly timescales, in addition to regions with memory effects and reduced response rates to external forcing. We find ecologically sensitive regions with amplified responses to climate variability in the Arctic tundra, parts of the boreal forest belt, the tropical rainforest, alpine regions worldwide, steppe and prairie regions of central Asia and North and South America, the Caatinga deciduous forest in eastern South America, and eastern areas of Australia. Our study provides a quantitative methodology for assessing the relative response rate of ecosystems--be they natural or with a strong anthropogenic signature--to environmental variability, which is the first step towards addressing why some regions appear to be more sensitive than others, and what impact this has on the resilience of ecosystem service provision and human well-being.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Seddon, Alistair W R -- Macias-Fauria, Marc -- Long, Peter R -- Benz, David -- Willis, Kathy J -- England -- Nature. 2016 Mar 10;531(7593):229-32. doi: 10.1038/nature16986. Epub 2016 Feb 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of Bergen, Allegaten 41, N-500 Bergen, Norway. ; School of Geography and the Environment, South Parks Road, University of Oxford, Oxford OX1 3QY, UK. ; Long-Term Ecology Laboratory, Biodiversity Institute, Oxford Martin School, Department of Zoology, South Parks Road, University of Oxford, Oxford OX1 3PS, UK. ; Royal Botanic Gardens, Kew, Richmond, Surrey TW9 3AB, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26886790" target="_blank"〉PubMed〈/a〉
    Keywords: *Acclimatization ; Americas ; Arctic Regions ; Asia ; Australia ; *Climate Change ; *Ecosystem ; Environmental Monitoring ; *Geographic Mapping ; Human Activities ; Models, Theoretical ; *Plant Physiological Phenomena ; Rainforest ; Temperature ; Time Factors ; Trees ; Water/analysis
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  • 58
    Publication Date: 2016-04-07
    Description: Neoplastic pancreatic epithelial cells are believed to die through caspase 8-dependent apoptotic cell death, and chemotherapy is thought to promote tumour apoptosis. Conversely, cancer cells often disrupt apoptosis to survive. Another type of programmed cell death is necroptosis (programmed necrosis), but its role in pancreatic ductal adenocarcinoma (PDA) is unclear. There are many potential inducers of necroptosis in PDA, including ligation of tumour necrosis factor receptor 1 (TNFR1), CD95, TNF-related apoptosis-inducing ligand (TRAIL) receptors, Toll-like receptors, reactive oxygen species, and chemotherapeutic drugs. Here we report that the principal components of the necrosome, receptor-interacting protein (RIP)1 and RIP3, are highly expressed in PDA and are further upregulated by the chemotherapy drug gemcitabine. Blockade of the necrosome in vitro promoted cancer cell proliferation and induced an aggressive oncogenic phenotype. By contrast, in vivo deletion of RIP3 or inhibition of RIP1 protected against oncogenic progression in mice and was associated with the development of a highly immunogenic myeloid and T cell infiltrate. The immune-suppressive tumour microenvironment associated with intact RIP1/RIP3 signalling depended in part on necroptosis-induced expression of the chemokine attractant CXCL1, and CXCL1 blockade protected against PDA. Moreover, cytoplasmic SAP130 (a subunit of the histone deacetylase complex) was expressed in PDA in a RIP1/RIP3-dependent manner, and Mincle--its cognate receptor--was upregulated in tumour-infiltrating myeloid cells. Ligation of Mincle by SAP130 promoted oncogenesis, whereas deletion of Mincle protected against oncogenesis and phenocopied the immunogenic reprogramming of the tumour microenvironment that was induced by RIP3 deletion. Cellular depletion suggested that whereas inhibitory macrophages promote tumorigenesis in PDA, they lose their immune-suppressive effects when RIP3 or Mincle is deleted. Accordingly, T cells, which are not protective against PDA progression in mice with intact RIP3 or Mincle signalling, are reprogrammed into indispensable mediators of anti-tumour immunity in the absence of RIP3 or Mincle. Our work describes parallel networks of necroptosis-induced CXCL1 and Mincle signalling that promote macrophage-induced adaptive immune suppression and thereby enable PDA progression.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4833566/" 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/PMC4833566/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Seifert, Lena -- Werba, Gregor -- Tiwari, Shaun -- Giao Ly, Nancy Ngoc -- Alothman, Sara -- Alqunaibit, Dalia -- Avanzi, Antonina -- Barilla, Rocky -- Daley, Donnele -- Greco, Stephanie H -- Torres-Hernandez, Alejandro -- Pergamo, Matthew -- Ochi, Atsuo -- Zambirinis, Constantinos P -- Pansari, Mridul -- Rendon, Mauricio -- Tippens, Daniel -- Hundeyin, Mautin -- Mani, Vishnu R -- Hajdu, Cristina -- Engle, Dannielle -- Miller, George -- CA155649/CA/NCI NIH HHS/ -- CA168611/CA/NCI NIH HHS/ -- CA193111/CA/NCI NIH HHS/ -- P30CA016087/CA/NCI NIH HHS/ -- R01 CA168611/CA/NCI NIH HHS/ -- T32 CA193111/CA/NCI NIH HHS/ -- UL1 TR000038/TR/NCATS NIH HHS/ -- England -- Nature. 2016 Apr 14;532(7598):245-9. doi: 10.1038/nature17403. Epub 2016 Apr 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉S. Arthur Localio Laboratory, Department of Surgery, New York University School of Medicine, 550 First Avenue, New York, New York 10016, USA. ; Department of Cell Biology, New York University School of Medicine, 550 First Avenue, New York, New York 10016, USA. ; Department of Pathology, New York University School of Medicine, 550 First Avenue, New York, New York 10016, USA. ; Cold Spring Harbor Laboratories, Cold Spring Harbor, New York 11724, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27049944" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/immunology/metabolism/pathology ; Animals ; Apoptosis/drug effects ; *Carcinogenesis/drug effects ; Carcinoma, Pancreatic Ductal/immunology/metabolism/pathology ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Chemokine CXCL1/antagonists & inhibitors/*metabolism ; Deoxycytidine/analogs & derivatives/pharmacology ; Disease Progression ; Female ; GTPase-Activating Proteins/metabolism ; Gene Expression Regulation, Neoplastic ; Humans ; *Immune Tolerance ; Lectins, C-Type/immunology/*metabolism ; Male ; Membrane Proteins/immunology/*metabolism ; Mice ; Mice, Inbred C57BL ; *Necrosis ; Pancreatic Neoplasms/*immunology/metabolism/*pathology ; Receptor-Interacting Protein Serine-Threonine Kinases/metabolism ; Signal Transduction ; Up-Regulation
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  • 59
    Publication Date: 2016-02-11
    Description: The enteric nervous system (ENS) is the largest component of the autonomic nervous system, with neuron numbers surpassing those present in the spinal cord. The ENS has been called the 'second brain' given its autonomy, remarkable neurotransmitter diversity and complex cytoarchitecture. Defects in ENS development are responsible for many human disorders including Hirschsprung disease (HSCR). HSCR is caused by the developmental failure of ENS progenitors to migrate into the gastrointestinal tract, particularly the distal colon. Human ENS development remains poorly understood owing to the lack of an easily accessible model system. Here we demonstrate the efficient derivation and isolation of ENS progenitors from human pluripotent stem (PS) cells, and their further differentiation into functional enteric neurons. ENS precursors derived in vitro are capable of targeted migration in the developing chick embryo and extensive colonization of the adult mouse colon. The in vivo engraftment and migration of human PS-cell-derived ENS precursors rescue disease-related mortality in HSCR mice (Ednrb(s-l/s-l)), although the mechanism of action remains unclear. Finally, EDNRB-null mutant ENS precursors enable modelling of HSCR-related migration defects, and the identification of pepstatin A as a candidate therapeutic target. Our study establishes the first, to our knowledge, human PS-cell-based platform for the study of human ENS development, and presents cell- and drug-based strategies for the treatment of HSCR.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4846424/" 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/PMC4846424/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fattahi, Faranak -- Steinbeck, Julius A -- Kriks, Sonja -- Tchieu, Jason -- Zimmer, Bastian -- Kishinevsky, Sarah -- Zeltner, Nadja -- Mica, Yvonne -- El-Nachef, Wael -- Zhao, Huiyong -- de Stanchina, Elisa -- Gershon, Michael D -- Grikscheit, Tracy C -- Chen, Shuibing -- Studer, Lorenz -- DP2 DK098093-01/DK/NIDDK NIH HHS/ -- NS15547/NS/NINDS NIH HHS/ -- P30 CA008748/CA/NCI NIH HHS/ -- R01 NS015547/NS/NINDS NIH HHS/ -- England -- Nature. 2016 Mar 3;531(7592):105-9. doi: 10.1038/nature16951. Epub 2016 Feb 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Center for Stem Cell Biology, New York, New York 10065, USA. ; Developmental Biology Program, Sloan-Kettering Institute for Cancer Research, New York, New York 10065, USA. ; Weill Graduate School of Medical Sciences of Cornell University, New York, New York 10065, USA. ; Molecular Pharmacology Program, New York, New York 10065, USA. ; Department of Pathology and Cell Biology, Columbia University, College of Physicians and Surgeons, New York, New York 10032, USA. ; Children's Hospital Los Angeles, Pediatric Surgery, Los Angeles, California 90027, USA. ; Department of Surgery, Weill Medical College of Cornell University, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26863197" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Cell Differentiation ; Cell Line ; *Cell Lineage ; Cell Movement ; Cell Separation ; *Cell- and Tissue-Based Therapy/methods ; Chick Embryo ; Colon/drug effects/pathology ; Disease Models, Animal ; Drug Discovery/*methods ; Enteric Nervous System/*pathology ; Female ; Gastrointestinal Tract/drug effects/pathology ; Hirschsprung Disease/*drug therapy/*pathology/therapy ; Humans ; Male ; Mice ; Neurons/drug effects/*pathology ; Pepstatins/metabolism ; Pluripotent Stem Cells/pathology ; Receptor, Endothelin B/metabolism ; Signal Transduction
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  • 60
    Publication Date: 2016-04-07
    Description: Microglia are damage sensors for the central nervous system (CNS), and the phagocytes responsible for routine non-inflammatory clearance of dead brain cells. Here we show that the TAM receptor tyrosine kinases Mer and Axl regulate these microglial functions. We find that adult mice deficient in microglial Mer and Axl exhibit a marked accumulation of apoptotic cells specifically in neurogenic regions of the CNS, and that microglial phagocytosis of the apoptotic cells generated during adult neurogenesis is normally driven by both TAM receptor ligands Gas6 and protein S. Using live two-photon imaging, we demonstrate that the microglial response to brain damage is also TAM-regulated, as TAM-deficient microglia display reduced process motility and delayed convergence to sites of injury. Finally, we show that microglial expression of Axl is prominently upregulated in the inflammatory environment that develops in a mouse model of Parkinson's disease. Together, these results establish TAM receptors as both controllers of microglial physiology and potential targets for therapeutic intervention in CNS disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fourgeaud, Lawrence -- Traves, Paqui G -- Tufail, Yusuf -- Leal-Bailey, Humberto -- Lew, Erin D -- Burrola, Patrick G -- Callaway, Perri -- Zagorska, Anna -- Rothlin, Carla V -- Nimmerjahn, Axel -- Lemke, Greg -- DP2 NS083038/DP/NCCDPHP CDC HHS/ -- DP2 NS083038/NS/NINDS NIH HHS/ -- P30CA014195/CA/NCI NIH HHS/ -- R01 AI089824/AI/NIAID NIH HHS/ -- R01 AI101400/AI/NIAID NIH HHS/ -- R01 NS085296/NS/NINDS NIH HHS/ -- R01 NS085938/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2016 Apr 14;532(7598):240-4. doi: 10.1038/nature17630. Epub 2016 Apr 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Neurobiology Laboratory, The Salk Institute for Biological Studies, La Jolla, California 92037, USA. ; Instituto de Investigaciones Biomedicas Alberto Sols (CSIC-UAM), Madrid 28029, Spain. ; Waitt Advanced Biophotonics Center, The Salk Institute for Biological Studies, La Jolla, California 92037, USA. ; Joint Master in Neuroscience Program, University of Strasbourg, Strasbourg 67081, France. ; Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA. ; Immunobiology and Microbial Pathogenesis Laboratory, The Salk Institute for Biological Studies, La Jolla, California 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27049947" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Brain/blood supply/cytology/*metabolism/pathology ; Brain Injuries/metabolism/pathology ; Disease Models, Animal ; Female ; Inflammation/metabolism ; Intercellular Signaling Peptides and Proteins/metabolism ; Ligands ; Male ; Mice ; Microglia/*physiology ; Neurogenesis ; Parkinson Disease/metabolism ; Phagocytosis ; Protein S/metabolism ; Proto-Oncogene Proteins/deficiency/*metabolism ; Receptor Protein-Tyrosine Kinases/deficiency/*metabolism ; Signal Transduction ; Stem Cell Niche ; Up-Regulation
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  • 61
    Publication Date: 2016-04-26
    Description: The evolution of novel cell types led to the emergence of new tissues and organs during the diversification of animals. The origin of the chondrocyte, the cell type that synthesizes cartilage matrix, was central to the evolution of the vertebrate endoskeleton. Cartilage-like tissues also exist outside the vertebrates, although their relationship to vertebrate cartilage is enigmatic. Here we show that protostome and deuterostome cartilage share structural and chemical properties, and that the mechanisms of cartilage development are extensively conserved--from induction of chondroprogenitor cells by Hedgehog and beta-catenin signalling, to chondrocyte differentiation and matrix synthesis by SoxE and SoxD regulation of clade A fibrillar collagen (ColA) genes--suggesting that the chondrogenic gene regulatory network evolved in the common ancestor of Bilateria. These results reveal deep homology of the genetic program for cartilage development in Bilateria and suggest that activation of this ancient core chondrogenic network underlies the parallel evolution of cartilage tissues in Ecdysozoa, Lophotrochozoa and Deuterostomia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tarazona, Oscar A -- Slota, Leslie A -- Lopez, Davys H -- Zhang, GuangJun -- Cohn, Martin J -- Howard Hughes Medical Institute/ -- England -- Nature. 2016 May 5;533(7601):86-9. doi: 10.1038/nature17398. Epub 2016 Apr 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, UF Genetics Institute, University of Florida, PO Box 103610, Gainesville, Florida 32610, USA. ; Department of Biology, University of Florida, PO Box 103610, Gainesville, Florida 32610, USA. ; Department of Molecular Genetics and Microbiology, University of Florida College of Medicine, PO Box 103610, Gainesville, Florida 32610, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27111511" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cartilage/anatomy & histology/embryology/metabolism ; Chondrocytes/cytology ; Chondrogenesis/*genetics ; Conserved Sequence/*genetics ; Decapodiformes/cytology/embryology/genetics/metabolism ; *Evolution, Molecular ; Fibrillar Collagens/genetics ; Gene Expression Regulation, Developmental/*genetics ; Gene Regulatory Networks ; Hedgehog Proteins/metabolism ; Invertebrates/cytology/*embryology/*genetics/metabolism ; *Phylogeny ; Signal Transduction ; Stem Cells/cytology ; Vertebrates/anatomy & histology/genetics ; beta Catenin/metabolism
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  • 62
    Publication Date: 2016-02-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ji, Weihong -- Aryal, Achyut -- Su, Junhu -- England -- Nature. 2016 Feb 4;530(7588):33. doi: 10.1038/530033c.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Massey University, Auckland, New Zealand; and Gansu Agricultural University, China. ; Gansu Agricultural University, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26842048" target="_blank"〉PubMed〈/a〉
    Keywords: Agriculture/instrumentation/legislation & jurisprudence ; Animal Migration ; Animals ; Animals, Wild/genetics/*physiology ; Conservation of Natural Resources/*legislation & jurisprudence/*methods ; *Ecosystem ; Environmental Policy/*legislation & jurisprudence ; Motor Vehicles ; Railroads ; Tibet
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  • 63
    Publication Date: 2016-03-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thingstad, T Frede -- Bratbak, Gunnar -- England -- Nature. 2016 Mar 24;531(7595):454-5. doi: 10.1038/nature17303. Epub 2016 Mar 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of Bergen, 5020 Bergen, Norway.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26982732" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anthozoa/*virology ; *Ecosystem ; *Host-Pathogen Interactions ; Viruses/*pathogenicity
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  • 64
    Publication Date: 2016-03-24
    Description: A marked bias towards risk aversion has been observed in nearly every species tested. A minority of individuals, however, instead seem to prefer risk (repeatedly choosing uncertain large rewards over certain but smaller rewards), and even risk-averse individuals sometimes opt for riskier alternatives. It is not known how neural activity underlies such important shifts in decision-making--either as a stable trait across individuals or at the level of variability within individuals. Here we describe a model of risk-preference in rats, in which stable individual differences, trial-by-trial choices, and responses to pharmacological agents all parallel human behaviour. By combining new genetic targeting strategies with optical recording of neural activity during behaviour in this model, we identify relevant temporally specific signals from a genetically and anatomically defined population of neurons. This activity occurred within dopamine receptor type-2 (D2R)-expressing cells in the nucleus accumbens (NAc), signalled unfavourable outcomes from the recent past at a time appropriate for influencing subsequent decisions, and also predicted subsequent choices made. Having uncovered this naturally occurring neural correlate of risk selection, we then mimicked the temporally specific signal with optogenetic control during decision-making and demonstrated its causal effect in driving risk-preference. Specifically, risk-preferring rats could be instantaneously converted to risk-averse rats with precisely timed phasic stimulation of NAc D2R cells. These findings suggest that individual differences in risk-preference, as well as real-time risky decision-making, can be largely explained by the encoding in D2R-expressing NAc cells of prior unfavourable outcomes during decision-making.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zalocusky, Kelly A -- Ramakrishnan, Charu -- Lerner, Talia N -- Davidson, Thomas J -- Knutson, Brian -- Deisseroth, Karl -- 1F31MH105151-01/MH/NIMH NIH HHS/ -- 1F32MH105053-01/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2016 Mar 31;531(7596):642-6. doi: 10.1038/nature17400. Epub 2016 Mar 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Bioengineering Department, Stanford University, Stanford, California 94305, USA. ; Neurosciences Program, Stanford University, Stanford, California 94305, USA. ; CNC Program, Stanford University, Stanford, California 94305, USA. ; Psychology Department, Stanford University, Stanford, California 94305, USA. ; Howard Hughes Medical Institute, Stanford University, Stanford, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27007845" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Choice Behavior ; *Decision Making ; Humans ; Individuality ; Male ; Models, Animal ; Models, Neurological ; Models, Psychological ; Neurons/*metabolism ; Nucleus Accumbens/*cytology/*metabolism ; Rats ; Rats, Long-Evans ; Receptors, Dopamine D2/*metabolism ; Reward ; *Risk Management ; Signal Transduction ; Uncertainty
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  • 65
    Publication Date: 2016-03-17
    Description: Microbial viruses can control host abundances via density-dependent lytic predator-prey dynamics. Less clear is how temperate viruses, which coexist and replicate with their host, influence microbial communities. Here we show that virus-like particles are relatively less abundant at high host densities. This suggests suppressed lysis where established models predict lytic dynamics are favoured. Meta-analysis of published viral and microbial densities showed that this trend was widespread in diverse ecosystems ranging from soil to freshwater to human lungs. Experimental manipulations showed viral densities more consistent with temperate than lytic life cycles at increasing microbial abundance. An analysis of 24 coral reef viromes showed a relative increase in the abundance of hallmark genes encoded by temperate viruses with increased microbial abundance. Based on these four lines of evidence, we propose the Piggyback-the-Winner model wherein temperate dynamics become increasingly important in ecosystems with high microbial densities; thus 'more microbes, fewer viruses'.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Knowles, B -- Silveira, C B -- Bailey, B A -- Barott, K -- Cantu, V A -- Cobian-Guemes, A G -- Coutinho, F H -- Dinsdale, E A -- Felts, B -- Furby, K A -- George, E E -- Green, K T -- Gregoracci, G B -- Haas, A F -- Haggerty, J M -- Hester, E R -- Hisakawa, N -- Kelly, L W -- Lim, Y W -- Little, M -- Luque, A -- McDole-Somera, T -- McNair, K -- de Oliveira, L S -- Quistad, S D -- Robinett, N L -- Sala, E -- Salamon, P -- Sanchez, S E -- Sandin, S -- Silva, G G Z -- Smith, J -- Sullivan, C -- Thompson, C -- Vermeij, M J A -- Youle, M -- Young, C -- Zgliczynski, B -- Brainard, R -- Edwards, R A -- Nulton, J -- Thompson, F -- Rohwer, F -- England -- Nature. 2016 Mar 24;531(7595):466-70. doi: 10.1038/nature17193. Epub 2016 Mar 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, San Diego State University, 5500 Campanile Drive, San Diego, California 92182, USA. ; Biology Institute, Rio de Janeiro Federal University, Av. Carlos Chagas Filho 373, Rio de Janeiro, Rio de Janeiro 21941-599, Brazil. ; Department of Mathematics and Statistics, San Diego State University, 5500 Campanile Drive, San Diego, California 92182, USA. ; Hawaii Institute of Marine Biology, University of Hawaii at Manoa, 46-007 Lilipuna Road, Kaneohe, Hawaii 96744, USA. ; Computational Science Research Center, San Diego State University, 5500 Campanile Drive, San Diego, California 92182, USA. ; Rainbow Rock, Ocean View, Hawaii 96737, USA. ; Radboud University Medical Centre, Radboud Institute for Molecular Life Sciences, Centre for Molecular and Biomolecular Informatics, 6525HP Nijmegen, The Netherlands. ; Viral Information Institute, San Diego State University, 5500 Campanile Drive, San Diego, California 92182, USA. ; Scripps Institution of Oceanography, 8622 Kennel Way, La Jolla, California 92037, USA. ; Department of Biology, University of California San Diego, 9500 Gilman Drive, La Jolla, California 92093, USA. ; Marine Sciences Department, Sao Paulo Federal University - Baixada Santista, Av. Alm. Saldanha da Gama, 89, Santos, Sao Paulo 11030-400, Brazil. ; National Geographic Society, 1145 17th St NW, Washington D.C. 20036, USA. ; CARMABI Foundation, Piscaderabaai z/n, Willemstad, Curacao, Netherlands Antilles. ; Aquatic Microbiology, Institute for Biodiversity and Ecosystem Dynamics, University of Amsterdam, 1098XH Amsterdam, The Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26982729" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anthozoa/physiology/*virology ; Bacteriophages/pathogenicity/physiology ; Coral Reefs ; *Ecosystem ; Genes, Viral/genetics ; *Host-Pathogen Interactions ; Lysogeny ; Models, Biological ; Virulence/genetics ; Viruses/genetics/isolation & purification/*pathogenicity
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  • 66
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    Nature Publishing Group (NPG)
    Publication Date: 2016-02-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wagner, Erwin F -- England -- Nature. 2016 Feb 4;530(7588):42-3. doi: 10.1038/530042a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Cancer Research Centre (CNIO), Department of Cancer Cell Biology, E-28029 Madrid, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26842052" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Disease Progression ; Fibroblasts/*cytology/*pathology ; I-kappa B Kinase/deficiency/genetics/metabolism ; Inflammation/immunology/pathology ; Intestinal Neoplasms/*immunology/*pathology/therapy ; Mice ; NF-kappa B/metabolism ; Signal Transduction ; Tumor Microenvironment/*physiology ; Uncertainty
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  • 67
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    Unknown
    Nature Publishing Group (NPG)
    Publication Date: 2016-04-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rodriguez, Barbra -- England -- Nature. 2016 Apr 21;532(7599):403-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27127819" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; Animal Migration ; Animals ; Biodiversity ; Climate Change/economics/*statistics & numerical data ; Ecology/economics/manpower/*methods/*trends ; *Ecosystem ; Plants ; Research/economics/manpower/*trends ; *Research Design ; Research Personnel ; *Uncertainty ; Ursidae ; *Weather
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  • 68
    Publication Date: 2016-04-14
    Description: Blood vessels define local microenvironments in the skeletal system, play crucial roles in osteogenesis and provide niches for haematopoietic stem cells. The properties of niche-forming vessels and their changes in the ageing organism remain incompletely understood. Here we show that Notch signalling in endothelial cells leads to the expansion of haematopoietic stem cell niches in bone, which involves increases in CD31-positive capillaries and platelet-derived growth factor receptor-beta (PDGFRbeta)-positive perivascular cells, arteriole formation and elevated levels of cellular stem cell factor. Although endothelial hypoxia-inducible factor signalling promotes some of these changes, it fails to enhance vascular niche function because of a lack of arterialization and expansion of PDGFRbeta-positive cells. In ageing mice, niche-forming vessels in the skeletal system are strongly reduced but can be restored by activation of endothelial Notch signalling. These findings indicate that vascular niches for haematopoietic stem cells are part of complex, age-dependent microenvironments involving multiple cell populations and vessel subtypes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kusumbe, Anjali P -- Ramasamy, Saravana K -- Itkin, Tomer -- Mae, Maarja Andaloussi -- Langen, Urs H -- Betsholtz, Christer -- Lapidot, Tsvee -- Adams, Ralf H -- England -- Nature. 2016 Apr 21;532(7599):380-4. doi: 10.1038/nature17638. Epub 2016 Apr 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck-Institute for Molecular Biomedicine, Department of Tissue Morphogenesis, and University of Munster, Faculty of Medicine, D-48149 Munster, Germany. ; Department of Immunology, The Weizmann Institute of Science, Rehovot 76100, Israel. ; Vascular Biology Program, Department of Immunology, Genetics and Pathology, Uppsala University, SE-751 85 Uppsala, Sweden. ; Department of Medical Biochemistry and Biophysics, Division of Vascular Biology, Karolinska Institute, Scheeles vag 2, SE-171 77 Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27074508" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*physiology ; Animals ; Antigens, CD31/metabolism ; Arterioles/cytology/*physiology ; Bone and Bones/*blood supply/cytology/metabolism ; Capillaries/cytology/*physiology ; Cell Count ; Endothelial Cells/metabolism ; Hematopoietic Stem Cells/*cytology ; Hypoxia-Inducible Factor 1/metabolism ; Male ; Mice ; Osteogenesis ; Receptor, Platelet-Derived Growth Factor beta/metabolism ; Receptors, Notch/metabolism ; Signal Transduction ; Stem Cell Factor/metabolism ; *Stem Cell Niche
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  • 69
    Publication Date: 2016-05-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Davis, Andrew R -- Broad, Allison -- England -- Nature. 2016 May 5;533(7601):36. doi: 10.1038/533036a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Wollongong, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27147022" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aquatic Organisms ; Biodiversity ; Conservation of Natural Resources/*methods/trends ; *Ecosystem ; Ships/*methods
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  • 70
    Publication Date: 2016-04-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Doherty, Tim S -- Maron, Martine -- England -- Nature. 2016 Mar 31;531(7596):580. doi: 10.1038/531580b.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Deakin University, Victoria, Australia. ; The University of Queensland, Brisbane, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27029269" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Australia ; *Ecosystem ; Endangered Species ; *Financing, Government ; *Fires/economics/statistics & numerical data ; Forests ; *Global Warming/economics/statistics & numerical data ; Leadership ; Politics ; Research/*economics/trends
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  • 71
    Publication Date: 2016-02-19
    Description: Resilience, a system's ability to adjust its activity to retain its basic functionality when errors, failures and environmental changes occur, is a defining property of many complex systems. Despite widespread consequences for human health, the economy and the environment, events leading to loss of resilience--from cascading failures in technological systems to mass extinctions in ecological networks--are rarely predictable and are often irreversible. These limitations are rooted in a theoretical gap: the current analytical framework of resilience is designed to treat low-dimensional models with a few interacting components, and is unsuitable for multi-dimensional systems consisting of a large number of components that interact through a complex network. Here we bridge this theoretical gap by developing a set of analytical tools with which to identify the natural control and state parameters of a multi-dimensional complex system, helping us derive effective one-dimensional dynamics that accurately predict the system's resilience. The proposed analytical framework allows us systematically to separate the roles of the system's dynamics and topology, collapsing the behaviour of different networks onto a single universal resilience function. The analytical results unveil the network characteristics that can enhance or diminish resilience, offering ways to prevent the collapse of ecological, biological or economic systems, and guiding the design of technological systems resilient to both internal failures and environmental changes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gao, Jianxi -- Barzel, Baruch -- Barabasi, Albert-Laszlo -- England -- Nature. 2016 Feb 18;530(7590):307-12. doi: 10.1038/nature16948.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Complex Network Research, Department of Physics, Northeastern University, Boston, Massachusetts 02115, USA. ; Department of Mathematics, Bar-Ilan University, Ramat-Gan 52900, Israel. ; Center for Cancer Systems Biology, Dana-Farber Cancer Institute, Harvard University, Boston, Massachusetts 02215, USA. ; Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA. ; Center for Network Science, Central European University, Budapest 1051, Hungary.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26887493" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; *Ecosystem ; Gene Expression Regulation ; Gene Regulatory Networks/*genetics ; *Models, Biological
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  • 72
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2016-09-09
    Description: Author: Jake Yeston
    Keywords: Inorganic Chemistry
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 73
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2016-08-16
    Description: Author: L. Bryan Ray
    Keywords: Signal Transduction
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    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 74
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2016-10-14
    Description: Authors: Caroline Ash, L. Bryan Ray
    Keywords: Signal Transduction
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    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 75
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2016-10-14
    Description: Reversible protein phosphorylation plays a fundamental role in signal transduction networks. Phosphorylation alters protein function by regulating enzymatic activity, stability, cellular localization, or binding partners. Over three-quarters of human proteins may be phosphorylated, with many targeted at multiple sites. Such multisite phosphorylation substantially increases the scope for modulating protein function—a protein with n phosphorylation sites has the potential to exist in 2n distinct phosphorylation states, each of which could, in theory, display modified functionality. Proteins can be substrates for several protein kinases, thereby integrating distinct signals to provide a coherent biological response. However, they can also be phosphorylated at multiple sites by a single protein kinase to promote a specific functional output that can be reversed by dephosphorylation by protein phosphatases. On page 233 of this issue, Mylona et al. (1) reveal an unexpected role for multisite phosphorylation, whereby a protein kinase progressively phosphorylates sites on a transcription factor to promote and then subsequently limit its activity independently of dephosphorylation. Authors: Alan J. Whitmarsh, Roger J. Davis
    Keywords: Signal Transduction
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  • 76
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2016-12-09
    Description: Author: Jake Yeston
    Keywords: Organic Chemistry
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    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 77
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2016-10-21
    Description: Author: Jake Yeston
    Keywords: Organic Chemistry
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    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 78
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2016-11-11
    Description: Author: Jake Yeston
    Keywords: Inorganic Chemistry
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  • 79
    Publication Date: 2015-05-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Limardo, Alexander J -- Worden, Alexandra Z -- England -- Nature. 2015 Jun 4;522(7554):36-7. doi: 10.1038/nature14530. Epub 2015 May 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ocean Sciences, University of California, Santa Cruz, California 95064, USA, and at the Monterey Bay Aquarium Research Institute, Moss Landing, California. ; 1] Department of Ocean Sciences, University of California, Santa Cruz, California 95064, USA, and at the Monterey Bay Aquarium Research Institute, Moss Landing, California. [2] Canadian Institute for Advanced Research, Toronto, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26017309" target="_blank"〉PubMed〈/a〉
    Keywords: Diatoms/*metabolism/*microbiology ; *Ecosystem ; Indoleacetic Acids/*metabolism ; Phytoplankton/*metabolism/*microbiology ; Rhodobacteraceae/*metabolism
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  • 80
    Publication Date: 2015-12-10
    Description: Epithelial regeneration is critical for barrier maintenance and organ function after intestinal injury. The intestinal stem cell (ISC) niche provides Wnt, Notch and epidermal growth factor (EGF) signals supporting Lgr5(+) crypt base columnar ISCs for normal epithelial maintenance. However, little is known about the regulation of the ISC compartment after tissue damage. Using ex vivo organoid cultures, here we show that innate lymphoid cells (ILCs), potent producers of interleukin-22 (IL-22) after intestinal injury, increase the growth of mouse small intestine organoids in an IL-22-dependent fashion. Recombinant IL-22 directly targeted ISCs, augmenting the growth of both mouse and human intestinal organoids, increasing proliferation and promoting ISC expansion. IL-22 induced STAT3 phosphorylation in Lgr5(+) ISCs, and STAT3 was crucial for both organoid formation and IL-22-mediated regeneration. Treatment with IL-22 in vivo after mouse allogeneic bone marrow transplantation enhanced the recovery of ISCs, increased epithelial regeneration and reduced intestinal pathology and mortality from graft-versus-host disease. ATOH1-deficient organoid culture demonstrated that IL-22 induced epithelial regeneration independently of the Paneth cell niche. Our findings reveal a fundamental mechanism by which the immune system is able to support the intestinal epithelium, activating ISCs to promote regeneration.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4720437/" 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/PMC4720437/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lindemans, Caroline A -- Calafiore, Marco -- Mertelsmann, Anna M -- O'Connor, Margaret H -- Dudakov, Jarrod A -- Jenq, Robert R -- Velardi, Enrico -- Young, Lauren F -- Smith, Odette M -- Lawrence, Gillian -- Ivanov, Juliet A -- Fu, Ya-Yuan -- Takashima, Shuichiro -- Hua, Guoqiang -- Martin, Maria L -- O'Rourke, Kevin P -- Lo, Yuan-Hung -- Mokry, Michal -- Romera-Hernandez, Monica -- Cupedo, Tom -- Dow, Lukas E -- Nieuwenhuis, Edward E -- Shroyer, Noah F -- Liu, Chen -- Kolesnick, Richard -- van den Brink, Marcel R M -- Hanash, Alan M -- HHSN272200900059C/PHS HHS/ -- K08 HL115355/HL/NHLBI NIH HHS/ -- K08-HL115355/HL/NHLBI NIH HHS/ -- K99 CA176376/CA/NCI NIH HHS/ -- K99-CA176376/CA/NCI NIH HHS/ -- P01 CA023766/CA/NCI NIH HHS/ -- P01-CA023766/CA/NCI NIH HHS/ -- P30 CA008748/CA/NCI NIH HHS/ -- P30-CA008748/CA/NCI NIH HHS/ -- R01 AI080455/AI/NIAID NIH HHS/ -- R01 AI100288/AI/NIAID NIH HHS/ -- R01 AI101406/AI/NIAID NIH HHS/ -- R01 HL069929/HL/NHLBI NIH HHS/ -- R01 HL125571/HL/NHLBI NIH HHS/ -- R01-AI080455/AI/NIAID NIH HHS/ -- R01-AI100288/AI/NIAID NIH HHS/ -- R01-AI101406/AI/NIAID NIH HHS/ -- R01-HL069929/HL/NHLBI NIH HHS/ -- R01-HL125571/HL/NHLBI NIH HHS/ -- U19 AI116497/AI/NIAID NIH HHS/ -- England -- Nature. 2015 Dec 24;528(7583):560-4. doi: 10.1038/nature16460. Epub 2015 Dec 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA. ; Department of Pediatrics, University Medical Center Utrecht, 3508 AB Utrecht, The Netherlands. ; Department of Immunology, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA. ; Department of Anatomy and Developmental Biology, Monash University, Clayton 3800, Australia. ; Department of Medicine, Weill Cornell Medicine, New York, New York 10021, USA. ; Department of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA. ; Department of Molecular Pharmacology, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA. ; Department of Cancer Biology &Genetics, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA. ; Department of Medicine, Baylor College of Medicine, Houston, Texas 77030, USA. ; Department of Hematology, Erasmus University Medical Center, 3000 CA Rotterdam, The Netherlands. ; Department of Pathology, Immunology and Laboratory Medicine, University of Florida College of Medicine, Gainesville, Florida 32610, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26649819" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Epithelial Cells/*cytology/immunology/pathology ; Female ; Graft vs Host Disease/pathology ; Humans ; Immunity, Mucosal ; Interleukins/deficiency/*immunology ; Intestinal Mucosa/*cytology/immunology/pathology ; Intestine, Small/*cytology/immunology/pathology ; Mice ; Organoids/cytology/growth & development/immunology ; Paneth Cells/cytology ; Phosphorylation ; *Regeneration ; STAT3 Transcription Factor/metabolism ; Signal Transduction ; Stem Cell Niche ; Stem Cells/*cytology/*metabolism
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  • 81
    Publication Date: 2015-07-15
    Description: Surface polysaccharides are important for bacterial interactions with multicellular organisms, and some are virulence factors in pathogens. In the legume-rhizobium symbiosis, bacterial exopolysaccharides (EPS) are essential for the development of infected root nodules. We have identified a gene in Lotus japonicus, Epr3, encoding a receptor-like kinase that controls this infection. We show that epr3 mutants are defective in perception of purified EPS, and that EPR3 binds EPS directly and distinguishes compatible and incompatible EPS in bacterial competition studies. Expression of Epr3 in epidermal cells within the susceptible root zone shows that the protein is involved in bacterial entry, while rhizobial and plant mutant studies suggest that Epr3 regulates bacterial passage through the plant's epidermal cell layer. Finally, we show that Epr3 expression is inducible and dependent on host perception of bacterial nodulation (Nod) factors. Plant-bacterial compatibility and bacterial access to legume roots is thus regulated by a two-stage mechanism involving sequential receptor-mediated recognition of Nod factor and EPS signals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kawaharada, Y -- Kelly, S -- Nielsen, M Wibroe -- Hjuler, C T -- Gysel, K -- Muszynski, A -- Carlson, R W -- Thygesen, M B -- Sandal, N -- Asmussen, M H -- Vinther, M -- Andersen, S U -- Krusell, L -- Thirup, S -- Jensen, K J -- Ronson, C W -- Blaise, M -- Radutoiu, S -- Stougaard, J -- England -- Nature. 2015 Jul 16;523(7560):308-12. doi: 10.1038/nature14611. Epub 2015 Jul 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Centre for Carbohydrate Recognition and Signalling. Aarhus University, Aarhus 8000 C, Denmark [2] Department of Molecular Biology and Genetics, Aarhus University, Aarhus 8000 C, Denmark. ; 1] Centre for Carbohydrate Recognition and Signalling. Aarhus University, Aarhus 8000 C, Denmark [2] Department of Molecular Biology and Genetics, Aarhus University, Aarhus 8000 C, Denmark [3] Department of Microbiology and Immunology, University of Otago, Dunedin 9054, New Zealand. ; 1] Centre for Carbohydrate Recognition and Signalling. Aarhus University, Aarhus 8000 C, Denmark [2] Department of Chemistry, University of Copenhagen, Frederiksberg 1871 C, Denmark. ; Complex Carbohydrate Research Center, University of Georgia, Athens, Georgia 30602, USA. ; 1] Centre for Carbohydrate Recognition and Signalling. Aarhus University, Aarhus 8000 C, Denmark [2] Department of Microbiology and Immunology, University of Otago, Dunedin 9054, New Zealand.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26153863" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Carbohydrate Sequence ; Lipopolysaccharides/chemistry/*metabolism ; Lotus/genetics/*metabolism/*microbiology ; Molecular Sequence Data ; Mutation/genetics ; Phenotype ; Plant Epidermis/metabolism/microbiology ; Plant Proteins/chemistry/genetics/*metabolism ; Plant Root Nodulation ; Protein Kinases/chemistry/genetics/metabolism ; Protein Structure, Tertiary ; Receptors, Cell Surface/chemistry/genetics/*metabolism ; Rhizobium/*metabolism ; Root Nodules, Plant/metabolism/microbiology ; Signal Transduction ; Species Specificity ; Suppression, Genetic/genetics ; *Symbiosis
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  • 82
    Publication Date: 2015-04-22
    Description: Impaired mitochondrial maintenance in disparate cell types is a shared hallmark of many human pathologies and ageing. How mitochondrial biogenesis coordinates with the removal of damaged or superfluous mitochondria to maintain cellular homeostasis is not well understood. Here we show that mitophagy, a selective type of autophagy targeting mitochondria for degradation, interfaces with mitochondrial biogenesis to regulate mitochondrial content and longevity in Caenorhabditis elegans. We find that DCT-1 is a key mediator of mitophagy and longevity assurance under conditions of stress in C. elegans. Impairment of mitophagy compromises stress resistance and triggers mitochondrial retrograde signalling through the SKN-1 transcription factor that regulates both mitochondrial biogenesis genes and mitophagy by enhancing DCT-1 expression. Our findings reveal a homeostatic feedback loop that integrates metabolic signals to coordinate the biogenesis and turnover of mitochondria. Uncoupling of these two processes during ageing contributes to overproliferation of damaged mitochondria and decline of cellular function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Palikaras, Konstantinos -- Lionaki, Eirini -- Tavernarakis, Nektarios -- England -- Nature. 2015 May 28;521(7553):525-8. doi: 10.1038/nature14300. Epub 2015 Apr 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Institute of Molecular Biology and Biotechnology, Foundation for Research and Technology - Hellas, Nikolaou Plastira 100, Heraklion 70013, Crete, Greece [2] Department of Biology, University of Crete, Heraklion 70013, Crete, Greece. ; Institute of Molecular Biology and Biotechnology, Foundation for Research and Technology - Hellas, Nikolaou Plastira 100, Heraklion 70013, Crete, Greece. ; 1] Institute of Molecular Biology and Biotechnology, Foundation for Research and Technology - Hellas, Nikolaou Plastira 100, Heraklion 70013, Crete, Greece [2] Department of Basic Sciences, Faculty of Medicine, University of Crete, Heraklion 71110, Crete, Greece.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25896323" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/pathology/*physiology ; Animals ; Caenorhabditis elegans/*cytology/genetics/*physiology ; Caenorhabditis elegans Proteins/metabolism ; DNA-Binding Proteins/metabolism ; Homeostasis ; Insulin/metabolism ; Insulin-Like Growth Factor I/metabolism ; Longevity ; Membrane Proteins/metabolism ; Mitochondria/genetics/*metabolism/pathology ; *Mitochondrial Degradation/genetics ; Signal Transduction ; Stress, Physiological ; Transcription Factors/metabolism
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  • 83
    Publication Date: 2015-05-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zanne, Amy E -- Tank, David C -- Cornwell, William K -- Eastman, Jonathan M -- Smith, Stephen A -- FitzJohn, Richard G -- McGlinn, Daniel J -- O'Meara, Brian C -- Moles, Angela T -- Reich, Peter B -- Royer, Dana L -- Soltis, Douglas E -- Stevens, Peter F -- Westoby, Mark -- Wright, Ian J -- Aarssen, Lonnie -- Bertin, Robert I -- Calaminus, Andre -- Govaerts, Rafael -- Hemmings, Frank -- Leishman, Michelle R -- Oleksyn, Jacek -- Soltis, Pamela S -- Swenson, Nathan G -- Warman, Laura -- Beaulieu, Jeremy M -- England -- Nature. 2015 May 21;521(7552):E6-7. doi: 10.1038/nature14394.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Biological Sciences, George Washington University, Washington DC 20052, USA. [2] Center for Conservation and Sustainable Development, Missouri Botanical Garden, St Louis, Missouri 63121, USA. ; 1] Department of Biological Sciences, University of Idaho, Moscow, Idaho 83844, USA. [2] Institute for Bioinformatics and Evolutionary Studies, University of Idaho, Moscow, Idaho 83844, USA. ; 1] Department of Ecological Sciences, Systems Ecology, de Boelelaan 1085, 1081 HV Amsterdam, The Netherlands. [2] Evolution &Ecology Research Centre, School of Biological, Earth and Environmental Sciences, University of New South Wales, Sydney, New South Wales 2052, Australia. ; Department of Ecology and Evolutionary Biology, University of Michigan, Ann Arbor, Michigan 48109, USA. ; 1] Department of Zoology and Biodiversity Research Centre, University of British Columbia, Vancouver, British Columbia V6T1Z4, Canada. [2] Department of Biological Sciences, Macquarie University, Sydney, New South Wales 2109, Australia. ; Department of Biology, College of Charleston, Charleston, South Carolina 29424, USA. ; Department of Ecology and Evolutionary Biology, University of Tennessee, Knoxville, Tennessee 37996, USA. ; Evolution &Ecology Research Centre, School of Biological, Earth and Environmental Sciences, University of New South Wales, Sydney, New South Wales 2052, Australia. ; 1] Department of Forest Resources, University of Minnesota, St Paul, Minnesota 55108, USA. [2] Hawkesbury Institute for the Environment, University of Western Sydney, Penrith, New South Wales 2751, Australia. ; Department of Earth and Environmental Sciences, Wesleyan University, Middletown, Connecticut 06459, USA. ; 1] Department of Biology, University of Florida, Gainesville, Florida 32611, USA. [2] Florida Museum of Natural History, University of Florida, Gainesville, Florida 32611, USA. [3] Genetics Institute, University of Florida, Gainesville, Florida 32611, USA. ; Department of Biology, University of Missouri-St Louis, St Louis, Missouri 63121, USA. ; Department of Biological Sciences, Macquarie University, Sydney, New South Wales 2109, Australia. ; Department of Biology, Queen's University, Kingston, Ontario K7L 3N6, Canada. ; Department of Biology, College of the Holy Cross, Worcester, Massachusetts 01610, USA. ; Department of Biology, University of Florida, Gainesville, Florida 32611, USA. ; Royal Botanic Gardens, Kew, Richmond TW9 3AB, UK. ; 1] Department of Forest Resources, University of Minnesota, St Paul, Minnesota 55108, USA. [2] Polish Academy of Sciences, Institute of Dendrology, 62-035 Kornik, Poland. ; 1] Florida Museum of Natural History, University of Florida, Gainesville, Florida 32611, USA. [2] Genetics Institute, University of Florida, Gainesville, Florida 32611, USA. ; Department of Plant Biology and Ecology, Evolutionary Biology and Behavior, Program, Michigan State University, East Lansing, Michigan 48824, USA. ; 1] Evolution &Ecology Research Centre, School of Biological, Earth and Environmental Sciences, University of New South Wales, Sydney, New South Wales 2052, Australia. [2] Institute of Pacific Islands Forestry, USDA Forest Service, Hilo, Hawaii 96720, USA. ; National Institute for Mathematical &Biological Synthesis, University of Tennessee, Knoxville, Tennessee 37996, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25993971" target="_blank"〉PubMed〈/a〉
    Keywords: Angiosperms/*anatomy & histology/*physiology ; *Biological Evolution ; *Cold Climate ; *Ecosystem ; *Freezing ; Xylem/*anatomy & histology
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  • 84
    Publication Date: 2015-02-20
    Description: Pluripotent stem cells provide a powerful system to dissect the underlying molecular dynamics that regulate cell fate changes during mammalian development. Here we report the integrative analysis of genome-wide binding data for 38 transcription factors with extensive epigenome and transcriptional data across the differentiation of human embryonic stem cells to the three germ layers. We describe core regulatory dynamics and show the lineage-specific behaviour of selected factors. In addition to the orchestrated remodelling of the chromatin landscape, we find that the binding of several transcription factors is strongly associated with specific loss of DNA methylation in one germ layer, and in many cases a reciprocal gain in the other layers. Taken together, our work shows context-dependent rewiring of transcription factor binding, downstream signalling effectors, and the epigenome during human embryonic stem cell differentiation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4499331/" 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/PMC4499331/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tsankov, Alexander M -- Gu, Hongcang -- Akopian, Veronika -- Ziller, Michael J -- Donaghey, Julie -- Amit, Ido -- Gnirke, Andreas -- Meissner, Alexander -- 5F32DK095537/DK/NIDDK NIH HHS/ -- P01 GM099117/GM/NIGMS NIH HHS/ -- P01GM099117/GM/NIGMS NIH HHS/ -- P50HG006193/HG/NHGRI NIH HHS/ -- U01 ES017155/ES/NIEHS NIH HHS/ -- U01ES017155/ES/NIEHS NIH HHS/ -- England -- Nature. 2015 Feb 19;518(7539):344-9. doi: 10.1038/nature14233.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA [2] Harvard Stem Cell Institute, Cambridge, Massachusetts 02138, USA [3] Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, Massachusetts 02138, USA. ; Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA. ; 1] Harvard Stem Cell Institute, Cambridge, Massachusetts 02138, USA [2] Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, Massachusetts 02138, USA. ; 1] Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA [2] Department of Immunology, Weizmann Institute, Rehovot, 76100 Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25693565" target="_blank"〉PubMed〈/a〉
    Keywords: *Cell Differentiation/genetics ; Cell Lineage ; Chromatin/chemistry/genetics/metabolism ; Chromatin Assembly and Disassembly/genetics ; DNA Methylation ; Embryonic Stem Cells/*cytology/*metabolism ; Enhancer Elements, Genetic/genetics ; Epigenesis, Genetic/genetics ; Epigenomics ; Genome, Human/genetics ; Germ Layers/cytology/metabolism ; Histones/chemistry/metabolism ; Humans ; Protein Binding ; Signal Transduction ; Transcription Factors/*metabolism ; Transcription, Genetic/genetics
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  • 85
    Publication Date: 2015-03-25
    Description: Wing polyphenism is an evolutionarily successful feature found in a wide range of insects. Long-winged morphs can fly, which allows them to escape adverse habitats and track changing resources, whereas short-winged morphs are flightless, but usually possess higher fecundity than the winged morphs. Studies on aphids, crickets and planthoppers have revealed that alternative wing morphs develop in response to various environmental cues, and that the response to these cues may be mediated by developmental hormones, although research in this area has yielded equivocal and conflicting results about exactly which hormones are involved. As it stands, the molecular mechanism underlying wing morph determination in insects has remained elusive. Here we show that two insulin receptors in the migratory brown planthopper Nilaparvata lugens, InR1 and InR2, have opposing roles in controlling long wing versus short wing development by regulating the activity of the forkhead transcription factor Foxo. InR1, acting via the phosphatidylinositol-3-OH kinase (PI(3)K)-protein kinase B (Akt) signalling cascade, leads to the long-winged morph if active and the short-winged morph if inactive. InR2, by contrast, functions as a negative regulator of the InR1-PI(3)K-Akt pathway: suppression of InR2 results in development of the long-winged morph. The brain-secreted ligand Ilp3 triggers development of long-winged morphs. Our findings provide the first evidence of a molecular basis for the regulation of wing polyphenism in insects, and they are also the first demonstration--to our knowledge--of binary control over alternative developmental outcomes, and thus deepen our understanding of the development and evolution of phenotypic plasticity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xu, Hai-Jun -- Xue, Jian -- Lu, Bo -- Zhang, Xue-Chao -- Zhuo, Ji-Chong -- He, Shu-Fang -- Ma, Xiao-Fang -- Jiang, Ya-Qin -- Fan, Hai-Wei -- Xu, Ji-Yu -- Ye, Yu-Xuan -- Pan, Peng-Lu -- Li, Qiao -- Bao, Yan-Yuan -- Nijhout, H Frederik -- Zhang, Chuan-Xi -- England -- Nature. 2015 Mar 26;519(7544):464-7. doi: 10.1038/nature14286. Epub 2015 Mar 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉State Key Laboratory of Rice Biology and Ministry of Agriculture Key Laboratory of Agricultural Entomology, Institute of Insect Sciences, Zhejiang University, Hangzhou 310058, China. ; Department of Biology, Duke University, Durham, North Carolina 27708, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25799997" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Forkhead Transcription Factors/deficiency/metabolism ; Hemiptera/*anatomy & histology/enzymology/genetics/*metabolism ; Insulin/metabolism ; Male ; Molecular Sequence Data ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Receptor, Insulin/deficiency/*metabolism ; Signal Transduction ; Wings, Animal/anatomy & histology/enzymology/*growth & development/*metabolism
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  • 86
    Publication Date: 2015-02-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pandolfi, John M -- England -- Nature. 2015 Feb 5;518(7537):43-4. doi: 10.1038/nature14196. Epub 2015 Jan 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Biological Sciences and the Australian Research Council Centre of Excellence for Coral Reef Studies, University of Queensland, Brisbane, Queensland 4072, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25652993" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anthozoa/*growth & development/*physiology ; *Climate Change ; *Coral Reefs ; *Ecosystem
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  • 87
    Publication Date: 2015-07-07
    Description: Stem cells integrate inputs from multiple sources. Stem cell niches provide signals that promote stem cell maintenance, while differentiated daughter cells are known to provide feedback signals to regulate stem cell replication and differentiation. Recently, stem cells have been shown to regulate themselves using an autocrine mechanism. The existence of a 'stem cell niche' was first postulated by Schofield in 1978 to define local environments necessary for the maintenance of haematopoietic stem cells. Since then, an increasing body of work has focused on defining stem cell niches. Yet little is known about how progenitor cell and differentiated cell numbers and proportions are maintained. In the airway epithelium, basal cells function as stem/progenitor cells that can both self-renew and produce differentiated secretory cells and ciliated cells. Secretory cells also act as transit-amplifying cells that eventually differentiate into post-mitotic ciliated cells . Here we describe a mode of cell regulation in which adult mammalian stem/progenitor cells relay a forward signal to their own progeny. Surprisingly, this forward signal is shown to be necessary for daughter cell maintenance. Using a combination of cell ablation, lineage tracing and signalling pathway modulation, we show that airway basal stem/progenitor cells continuously supply a Notch ligand to their daughter secretory cells. Without these forward signals, the secretory progenitor cell pool fails to be maintained and secretory cells execute a terminal differentiation program and convert into ciliated cells. Thus, a parent stem/progenitor cell can serve as a functional daughter cell niche.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4521991/" 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/PMC4521991/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pardo-Saganta, Ana -- Tata, Purushothama Rao -- Law, Brandon M -- Saez, Borja -- Chow, Ryan Dz-Wei -- Prabhu, Mythili -- Gridley, Thomas -- Rajagopal, Jayaraj -- 5P30HL101287-02/HL/NHLBI NIH HHS/ -- R01 HL118185/HL/NHLBI NIH HHS/ -- R01HL118185/HL/NHLBI NIH HHS/ -- England -- Nature. 2015 Jul 30;523(7562):597-601. doi: 10.1038/nature14553. Epub 2015 Jul 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Center for Regenerative Medicine, Massachusetts General Hospital, 185 Cambridge Street, Boston, Massachusetts 02114, USA [2] Departments of Internal Medicine and Pediatrics, Pulmonary and Critical Care Unit, Massachusetts General Hospital, Boston, Massachusetts 02114, USA [3] Harvard Stem Cell Institute, Cambridge, Massachusetts 02138, USA. ; 1] Center for Regenerative Medicine, Massachusetts General Hospital, 185 Cambridge Street, Boston, Massachusetts 02114, USA [2] Harvard Stem Cell Institute, Cambridge, Massachusetts 02138, USA [3] Stem Cell and Regenerative Biology Department, Harvard University, Cambridge, Massachusetts 02138, USA. ; Center for Molecular Medicine, Maine Medical Center Research Institute, 81 Research Drive, Scarborough, Maine 04074, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26147083" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Communication ; Cell Differentiation ; Cell Division ; Cilia/metabolism ; Female ; Male ; Membrane Proteins/metabolism ; Mice ; Receptor, Notch2/metabolism ; Signal Transduction ; Stem Cell Niche/*physiology ; Stem Cells/*cytology/metabolism/secretion ; Trachea/cytology
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  • 88
    Publication Date: 2015-04-10
    Description: Continuing degradation of coral reef ecosystems has generated substantial interest in how management can support reef resilience. Fishing is the primary source of diminished reef function globally, leading to widespread calls for additional marine reserves to recover fish biomass and restore key ecosystem functions. Yet there are no established baselines for determining when these conservation objectives have been met or whether alternative management strategies provide similar ecosystem benefits. Here we establish empirical conservation benchmarks and fish biomass recovery timelines against which coral reefs can be assessed and managed by studying the recovery potential of more than 800 coral reefs along an exploitation gradient. We show that resident reef fish biomass in the absence of fishing (B0) averages approximately 1,000 kg ha(-1), and that the vast majority (83%) of fished reefs are missing more than half their expected biomass, with severe consequences for key ecosystem functions such as predation. Given protection from fishing, reef fish biomass has the potential to recover within 35 years on average and less than 60 years when heavily depleted. Notably, alternative fisheries restrictions are largely (64%) successful at maintaining biomass above 50% of B0, sustaining key functions such as herbivory. Our results demonstrate that crucial ecosystem functions can be maintained through a range of fisheries restrictions, allowing coral reef managers to develop recovery plans that meet conservation and livelihood objectives in areas where marine reserves are not socially or politically feasible solutions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉MacNeil, M Aaron -- Graham, Nicholas A J -- Cinner, Joshua E -- Wilson, Shaun K -- Williams, Ivor D -- Maina, Joseph -- Newman, Steven -- Friedlander, Alan M -- Jupiter, Stacy -- Polunin, Nicholas V C -- McClanahan, Tim R -- England -- Nature. 2015 Apr 16;520(7547):341-4. doi: 10.1038/nature14358. Epub 2015 Apr 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Australian Institute of Marine Science, PMB 3 Townsville MC, Townsville, Queensland 4810, Australia [2] Department of Mathematics and Statistics, Dalhousie University, Halifax, Nova Scotia B3H 3J5, Canada [3] Australian Research Council Centre of Excellence for Coral Reef Studies, James Cook University, Townsville, Queensland 4811, Australia. ; Australian Research Council Centre of Excellence for Coral Reef Studies, James Cook University, Townsville, Queensland 4811, Australia. ; 1] Department of Parks and Wildlife, Kensington, Perth, Western Australia 6151, Australia [2] Oceans Institute, University of Western Australia, Crawley, Western Australia 6009, Australia. ; Coral Reef Ecosystems Division, NOAA Pacific Islands Fisheries Science Center, Honolulu, Hawaii 96818, USA. ; 1] Australian Research Council Centre of Excellence for Environmental Decisions (CEED), University of Queensland, Brisbane, St Lucia, Queensland 4074, Australia [2] Wildlife Conservation Society, Marine Programs, Bronx, New York 10460, USA. ; School of Marine Science and Technology, Newcastle University, Newcastle upon Tyne NE1 7RU, UK. ; 1] Fisheries Ecology Research Lab, Department of Biology, University of Hawaii, Honolulu, Hawaii 96822, USA [2] Pristine Seas-National Geographic, Washington DC 20036, USA. ; Wildlife Conservation Society, Marine Programs, Bronx, New York 10460, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25855298" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biodiversity ; Biomass ; Conservation of Natural Resources/*methods/statistics & numerical data/*trends ; *Coral Reefs ; *Ecosystem ; Fisheries/*methods/standards/*statistics & numerical data ; Fishes/*physiology ; Herbivory ; Population Dynamics ; Predatory Behavior ; Time Factors
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  • 89
    Publication Date: 2015-06-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Magnan, Alexandre -- Duvat, Virginie -- England -- Nature. 2015 Jun 11;522(7555):156. doi: 10.1038/522156b.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Sustainable Development and International Relations (IDDRI), Sciences Po, Paris, France. ; Littoral, Environment and Societies Research Unit (LIENSs, UMR 7266), University of La Rochelle and CNRS, La Rochelle, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26062500" target="_blank"〉PubMed〈/a〉
    Keywords: Agriculture ; Animals ; Anthozoa ; *Ecosystem ; Fisheries ; Mining/*legislation & jurisprudence ; Pacific Ocean ; Phosphates/*isolation & purification ; Polynesia
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  • 90
    Publication Date: 2015-09-17
    Description: Blood polymorphonuclear neutrophils provide immune protection against pathogens, but may also promote tissue injury in inflammatory diseases. Although neutrophils are generally considered to be a relatively homogeneous population, evidence for heterogeneity is emerging. Under steady-state conditions, neutrophil heterogeneity may arise from ageing and replenishment by newly released neutrophils from the bone marrow. Aged neutrophils upregulate CXCR4, a receptor allowing their clearance in the bone marrow, with feedback inhibition of neutrophil production via the IL-17/G-CSF axis, and rhythmic modulation of the haematopoietic stem-cell niche. The aged subset also expresses low levels of L-selectin. Previous studies have suggested that in vitro-aged neutrophils exhibit impaired migration and reduced pro-inflammatory properties. Here, using in vivo ageing analyses in mice, we show that neutrophil pro-inflammatory activity correlates positively with their ageing whilst in circulation. Aged neutrophils represent an overly active subset exhibiting enhanced alphaMbeta2 integrin activation and neutrophil extracellular trap formation under inflammatory conditions. Neutrophil ageing is driven by the microbiota via Toll-like receptor and myeloid differentiation factor 88-mediated signalling pathways. Depletion of the microbiota significantly reduces the number of circulating aged neutrophils and dramatically improves the pathogenesis and inflammation-related organ damage in models of sickle-cell disease or endotoxin-induced septic shock. These results identify a role for the microbiota in regulating a disease-promoting neutrophil subset.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4712631/" 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/PMC4712631/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Dachuan -- Chen, Grace -- Manwani, Deepa -- Mortha, Arthur -- Xu, Chunliang -- Faith, Jeremiah J -- Burk, Robert D -- Kunisaki, Yuya -- Jang, Jung-Eun -- Scheiermann, Christoph -- Merad, Miriam -- Frenette, Paul S -- R01 CA154947/CA/NCI NIH HHS/ -- R01 CA173861/CA/NCI NIH HHS/ -- R01 CA190400/CA/NCI NIH HHS/ -- R01 DK056638/DK/NIDDK NIH HHS/ -- R01 HL069438/HL/NHLBI NIH HHS/ -- R01 HL116340/HL/NHLBI NIH HHS/ -- England -- Nature. 2015 Sep 24;525(7570):528-32. doi: 10.1038/nature15367. Epub 2015 Sep 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ruth L. and David S. Gottesman Institute for Stem Cell and Regenerative Medicine Research, Albert Einstein College of Medicine, Bronx, New York 10461, USA. ; Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York 10461, USA. ; Department of Pediatrics, Albert Einstein College of Medicine, Bronx, New York 10461, USA. ; Department of Oncological Sciences, Mount Sinai School of Medicine, New York, New York 10029, USA. ; The Immunology Institute, Mount Sinai School of Medicine, New York, New York 10029, USA. ; The Institute for Genomics and Multiscale Biology, Mount Sinai School of Medicine, New York, New York 10029, USA. ; Department of Medicine, Albert Einstein College of Medicine, Bronx, New York 10461, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26374999" target="_blank"〉PubMed〈/a〉
    Keywords: Anemia, Sickle Cell/blood/microbiology/pathology ; Animals ; Cell Aging/*immunology ; Disease Models, Animal ; Erythrocytes, Abnormal/pathology ; Inflammation/immunology/pathology ; Macrophage-1 Antigen/metabolism ; Male ; Mice ; Microbiota/*immunology ; Myeloid Differentiation Factor 88/metabolism ; Neutrophils/*cytology/*immunology ; Shock, Septic/immunology/microbiology/pathology ; Signal Transduction ; Toll-Like Receptors/immunology
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  • 91
    Publication Date: 2015-06-18
    Description: Cell-to-cell variation is a universal feature of life that affects a wide range of biological phenomena, from developmental plasticity to tumour heterogeneity. Although recent advances have improved our ability to document cellular phenotypic variation, the fundamental mechanisms that generate variability from identical DNA sequences remain elusive. Here we reveal the landscape and principles of mammalian DNA regulatory variation by developing a robust method for mapping the accessible genome of individual cells by assay for transposase-accessible chromatin using sequencing (ATAC-seq) integrated into a programmable microfluidics platform. Single-cell ATAC-seq (scATAC-seq) maps from hundreds of single cells in aggregate closely resemble accessibility profiles from tens of millions of cells and provide insights into cell-to-cell variation. Accessibility variance is systematically associated with specific trans-factors and cis-elements, and we discover combinations of trans-factors associated with either induction or suppression of cell-to-cell variability. We further identify sets of trans-factors associated with cell-type-specific accessibility variance across eight cell types. Targeted perturbations of cell cycle or transcription factor signalling evoke stimulus-specific changes in this observed variability. The pattern of accessibility variation in cis across the genome recapitulates chromosome compartments de novo, linking single-cell accessibility variation to three-dimensional genome organization. Single-cell analysis of DNA accessibility provides new insight into cellular variation of the 'regulome'.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4685948/" 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/PMC4685948/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Buenrostro, Jason D -- Wu, Beijing -- Litzenburger, Ulrike M -- Ruff, Dave -- Gonzales, Michael L -- Snyder, Michael P -- Chang, Howard Y -- Greenleaf, William J -- 5U54HG00455805/HG/NHGRI NIH HHS/ -- P50 HG007735/HG/NHGRI NIH HHS/ -- P50HG007735/HG/NHGRI NIH HHS/ -- T32 HG000044/HG/NHGRI NIH HHS/ -- T32HG000044/HG/NHGRI NIH HHS/ -- U19 AI057266/AI/NIAID NIH HHS/ -- U19AI057266/AI/NIAID NIH HHS/ -- U54 HG004558/HG/NHGRI NIH HHS/ -- UH2 AR067676/AR/NIAMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2015 Jul 23;523(7561):486-90. doi: 10.1038/nature14590. Epub 2015 Jun 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Genetics, Stanford University School of Medicine, Stanford, California 94305, USA [2] Program in Epithelial Biology and the Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, California 94305, USA. ; Department of Genetics, Stanford University School of Medicine, Stanford, California 94305, USA. ; Program in Epithelial Biology and the Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, California 94305, USA. ; Fluidigm Corporation, South San Francisco, California 94080, USA. ; 1] Department of Genetics, Stanford University School of Medicine, Stanford, California 94305, USA [2] Department of Applied Physics, Stanford University, Stanford, California 94025, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26083756" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Compartmentation ; Cell Cycle/genetics ; Cell Line ; Cells/classification/*metabolism ; Chromatin/*genetics/*metabolism ; DNA/genetics/metabolism ; Epigenesis, Genetic ; *Epigenomics ; Genome, Human/genetics ; Humans ; Microfluidics ; Signal Transduction ; Single-Cell Analysis/*methods ; Transcription Factors/metabolism ; Transposases/metabolism
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  • 92
    Publication Date: 2015-01-22
    Description: Climate-induced coral bleaching is among the greatest current threats to coral reefs, causing widespread loss of live coral cover. Conditions under which reefs bounce back from bleaching events or shift from coral to algal dominance are unknown, making it difficult to predict and plan for differing reef responses under climate change. Here we document and predict long-term reef responses to a major climate-induced coral bleaching event that caused unprecedented region-wide mortality of Indo-Pacific corals. Following loss of 〉90% live coral cover, 12 of 21 reefs recovered towards pre-disturbance live coral states, while nine reefs underwent regime shifts to fleshy macroalgae. Functional diversity of associated reef fish communities shifted substantially following bleaching, returning towards pre-disturbance structure on recovering reefs, while becoming progressively altered on regime shifting reefs. We identified threshold values for a range of factors that accurately predicted ecosystem response to the bleaching event. Recovery was favoured when reefs were structurally complex and in deeper water, when density of juvenile corals and herbivorous fishes was relatively high and when nutrient loads were low. Whether reefs were inside no-take marine reserves had no bearing on ecosystem trajectory. Although conditions governing regime shift or recovery dynamics were diverse, pre-disturbance quantification of simple factors such as structural complexity and water depth accurately predicted ecosystem trajectories. These findings foreshadow the likely divergent but predictable outcomes for reef ecosystems in response to climate change, thus guiding improved management and adaptation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Graham, Nicholas A J -- Jennings, Simon -- MacNeil, M Aaron -- Mouillot, David -- Wilson, Shaun K -- England -- Nature. 2015 Feb 5;518(7537):94-7. doi: 10.1038/nature14140. Epub 2015 Jan 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Australian Research Council Centre of Excellence for Coral Reef Studies, James Cook University, Townsville, Queensland 4811 Australia. ; 1] Centre for Environment, Fisheries and Aquaculture Science, Pakefield Road, Lowestoft NR33 OHT, UK [2] School of Environmental Sciences, University of East Anglia, Norwich NR4 7TJ, UK. ; 1] Australian Research Council Centre of Excellence for Coral Reef Studies, James Cook University, Townsville, Queensland 4811 Australia [2] Australian Institute of Marine Science, PMB 3 Townsville MC, Townsville, Queensland 4810, Australia. ; 1] Australian Research Council Centre of Excellence for Coral Reef Studies, James Cook University, Townsville, Queensland 4811 Australia [2] ECOSYM, UMR CNRS-UM2 5119, Universite Montpellier 2, 34095 Montpellier Cedex, France. ; 1] Department of Parks and Wildlife, Kensington, Perth, Western Australia 6151, Australia [2] School of Plant Biology, Oceans Institute, University of Western Australia, Crawley, Western Australia 6009, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25607371" target="_blank"〉PubMed〈/a〉
    Keywords: Acclimatization ; Animals ; Anthozoa/*growth & development/*physiology ; Biodiversity ; *Climate Change ; *Coral Reefs ; *Ecosystem ; Fishes/physiology ; Indian Ocean ; Pacific Ocean ; Population Dynamics ; Seawater/analysis ; Seaweed/physiology ; Seychelles ; Symbiosis ; Tropical Climate
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    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 93
    Publication Date: 2015-02-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Di Lorenzo, Emanuele -- England -- Nature. 2015 Feb 19;518(7539):310-1. doi: 10.1038/518310a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Earth and Atmospheric Sciences, Georgia Institute of Technology, Atlanta, Georgia 30332-0340, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25693560" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Climate Change ; *Ecosystem ; *Water Movements
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 94
    Publication Date: 2015-06-23
    Description: Although the adult mammalian heart is incapable of meaningful functional recovery following substantial cardiomyocyte loss, it is now clear that modest cardiomyocyte turnover occurs in adult mouse and human hearts, mediated primarily by proliferation of pre-existing cardiomyocytes. However, fate mapping of these cycling cardiomyocytes has not been possible thus far owing to the lack of identifiable genetic markers. In several organs, stem or progenitor cells reside in relatively hypoxic microenvironments where the stabilization of the hypoxia-inducible factor 1 alpha (Hif-1alpha) subunit is critical for their maintenance and function. Here we report fate mapping of hypoxic cells and their progenies by generating a transgenic mouse expressing a chimaeric protein in which the oxygen-dependent degradation (ODD) domain of Hif-1alpha is fused to the tamoxifen-inducible CreERT2 recombinase. In mice bearing the creERT2-ODD transgene driven by either the ubiquitous CAG promoter or the cardiomyocyte-specific alpha myosin heavy chain promoter, we identify a rare population of hypoxic cardiomyocytes that display characteristics of proliferative neonatal cardiomyocytes, such as smaller size, mononucleation and lower oxidative DNA damage. Notably, these hypoxic cardiomyocytes contributed widely to new cardiomyocyte formation in the adult heart. These results indicate that hypoxia signalling is an important hallmark of cycling cardiomyocytes, and suggest that hypoxia fate mapping can be a powerful tool for identifying cycling cells in adult mammals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kimura, Wataru -- Xiao, Feng -- Canseco, Diana C -- Muralidhar, Shalini -- Thet, SuWannee -- Zhang, Helen M -- Abderrahman, Yezan -- Chen, Rui -- Garcia, Joseph A -- Shelton, John M -- Richardson, James A -- Ashour, Abdelrahman M -- Asaithamby, Aroumougame -- Liang, Hanquan -- Xing, Chao -- Lu, Zhigang -- Zhang, Cheng Cheng -- Sadek, Hesham A -- I01 BX000446/BX/BLRD VA/ -- R01 HL108104/HL/NHLBI NIH HHS/ -- England -- Nature. 2015 Jul 9;523(7559):226-30. doi: 10.1038/nature14582. Epub 2015 Jun 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Internal Medicine, Division of Cardiology, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA [2] Life Science Center, Tsukuba Advanced Research Alliance, University of Tsukuba, 1-1-1 Tennoudai, Tsukuba, Ibaraki 305-8577, Japan. ; Department of Internal Medicine, Division of Cardiology, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. ; Departments of Physiology and Developmental Biology, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. ; 1] Department of Internal Medicine, Division of Cardiology, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA [2] Department of Medicine, VA North Texas Health Care System, 4600 South Lancaster Road, Dallas, Texas 75216, USA. ; 1] Department of Molecular Biology, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA [2] Department of Pathology, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. ; Department of Radiation Oncology, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. ; McDermott Center for Human Growth and Development, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. ; 1] Department of Internal Medicine, Division of Cardiology, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA [2] Hamon Center for Regenerative Science and Medicine, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26098368" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Hypoxia ; Cell Proliferation/genetics ; Female ; Hypoxia-Inducible Factor 1, alpha Subunit/genetics/metabolism ; Male ; Mice ; Mice, Transgenic ; Myocardium/*cytology ; Myocytes, Cardiac/*cytology/metabolism ; Protein Structure, Tertiary ; Recombinant Fusion Proteins/genetics/*metabolism ; Recombinases/genetics/metabolism ; Signal Transduction ; Stem Cells/cytology/metabolism
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  • 95
    Publication Date: 2015-03-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kotiaho, Janne S -- England -- Nature. 2015 Mar 5;519(7541):33. doi: 10.1038/519033a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Jyvaskyla, Finland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25739622" target="_blank"〉PubMed〈/a〉
    Keywords: Biodiversity ; Conservation of Natural Resources/*methods/*statistics & numerical data ; *Ecosystem ; Finland ; Forestry/methods/statistics & numerical data ; Forests
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 96
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    Nature Publishing Group (NPG)
    Publication Date: 2015-12-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Massante, Jhonny Capichoni -- England -- Nature. 2015 Dec 3;528(7580):39. doi: 10.1038/528039c.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Federal University Fluminense, Niteroi, Rio de Janeiro, Brazil.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26632581" target="_blank"〉PubMed〈/a〉
    Keywords: Biodiversity ; Cities ; *Disasters/prevention & control ; *Ecosystem ; Humans ; *Mining ; Rainforest ; Water Pollutants/*adverse effects ; Water Supply
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 97
    Publication Date: 2015-05-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Edwards, Erika J -- de Vos, Jurriaan M -- Donoghue, Michael J -- England -- Nature. 2015 May 21;521(7552):E5-6. doi: 10.1038/nature14393.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ecology and Evolutionary Biology, Brown University, 80 Waterman St, Box G-W, Providence, Rhodes Island 02912, USA. ; Department of Ecology and Evolutionary Biology, Yale University, PO Box 208105, New Haven, Connecticut 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25993970" target="_blank"〉PubMed〈/a〉
    Keywords: Angiosperms/*anatomy & histology/*physiology ; *Biological Evolution ; *Cold Climate ; *Ecosystem ; *Freezing ; Xylem/*anatomy & histology
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  • 98
    Publication Date: 2015-03-18
    Description: Vertebrates have a unique 3D body shape in which correct tissue and organ shape and alignment are essential for function. For example, vision requires the lens to be centred in the eye cup which must in turn be correctly positioned in the head. Tissue morphogenesis depends on force generation, force transmission through the tissue, and response of tissues and extracellular matrix to force. Although a century ago D'Arcy Thompson postulated that terrestrial animal body shapes are conditioned by gravity, there has been no animal model directly demonstrating how the aforementioned mechano-morphogenetic processes are coordinated to generate a body shape that withstands gravity. Here we report a unique medaka fish (Oryzias latipes) mutant, hirame (hir), which is sensitive to deformation by gravity. hir embryos display a markedly flattened body caused by mutation of YAP, a nuclear executor of Hippo signalling that regulates organ size. We show that actomyosin-mediated tissue tension is reduced in hir embryos, leading to tissue flattening and tissue misalignment, both of which contribute to body flattening. By analysing YAP function in 3D spheroids of human cells, we identify the Rho GTPase activating protein ARHGAP18 as an effector of YAP in controlling tissue tension. Together, these findings reveal a previously unrecognised function of YAP in regulating tissue shape and alignment required for proper 3D body shape. Understanding this morphogenetic function of YAP could facilitate the use of embryonic stem cells to generate complex organs requiring correct alignment of multiple tissues.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4720436/" 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/PMC4720436/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Porazinski, Sean -- Wang, Huijia -- Asaoka, Yoichi -- Behrndt, Martin -- Miyamoto, Tatsuo -- Morita, Hitoshi -- Hata, Shoji -- Sasaki, Takashi -- Krens, S F Gabriel -- Osada, Yumi -- Asaka, Satoshi -- Momoi, Akihiro -- Linton, Sarah -- Miesfeld, Joel B -- Link, Brian A -- Senga, Takeshi -- Castillo-Morales, Atahualpa -- Urrutia, Araxi O -- Shimizu, Nobuyoshi -- Nagase, Hideaki -- Matsuura, Shinya -- Bagby, Stefan -- Kondoh, Hisato -- Nishina, Hiroshi -- Heisenberg, Carl-Philipp -- Furutani-Seiki, Makoto -- P30 EY001931/EY/NEI NIH HHS/ -- R01 EY014167/EY/NEI NIH HHS/ -- R01 EY016060/EY/NEI NIH HHS/ -- R01EY014167/EY/NEI NIH HHS/ -- Medical Research Council/United Kingdom -- England -- Nature. 2015 May 14;521(7551):217-21. doi: 10.1038/nature14215. Epub 2015 Mar 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology and Biochemistry, University of Bath, Bath BA2 7AY, UK. ; Department of Developmental and Regenerative Biology, Medical Research Institute, Tokyo Medical and Dental University (TMDU), Tokyo 113-8510, Japan. ; IST Austria, Am Campus 1, A-3400 Klosterneuburg, Austria. ; Department of Genetics and Cell Biology, Research Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima 734-8553, Japan. ; Department of Molecular Biology, School of Medicine, Keio University, Tokyo 160-8582, Japan. ; Japan Science and Technology Agency (JST), ERATO-SORST Kondoh Differentiation Signaling Project, Kyoto 606-8305, Japan. ; Department of Cell Biology, Neurobiology, and Anatomy, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA. ; Division of Cancer Biology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan. ; Kennedy Institute of Rheumatology, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, University of Oxford, Oxford OX3 7FY, UK. ; 1] Japan Science and Technology Agency (JST), ERATO-SORST Kondoh Differentiation Signaling Project, Kyoto 606-8305, Japan [2] Graduate School of Frontier Bioscience, Osaka University, Osaka 565-0871, Japan [3] Faculty of Life Sciences, Kyoto Sangyo University, Kyoto 603-8555, Japan. ; 1] Department of Biology and Biochemistry, University of Bath, Bath BA2 7AY, UK [2] Japan Science and Technology Agency (JST), ERATO-SORST Kondoh Differentiation Signaling Project, Kyoto 606-8305, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25778702" target="_blank"〉PubMed〈/a〉
    Keywords: Actomyosin/metabolism ; Adaptor Proteins, Signal Transducing/genetics/metabolism ; Animals ; Body Size/*genetics ; Embryo, Nonmammalian/anatomy & histology/embryology/metabolism ; Fish Proteins/genetics/*metabolism ; GTPase-Activating Proteins/metabolism ; Genes, Essential/genetics ; Gravitation ; Humans ; Morphogenesis/*genetics ; Mutation/genetics ; Organ Size/genetics ; Oryzias/*anatomy & histology/*embryology/genetics ; Phenotype ; Protein-Serine-Threonine Kinases/genetics/metabolism ; Signal Transduction ; Spheroids, Cellular/cytology/metabolism
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  • 99
    Publication Date: 2015-04-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dulvy, Nicholas K -- Kindsvater, Holly K -- England -- Nature. 2015 Apr 16;520(7547):304-5. doi: 10.1038/nature14384. Epub 2015 Apr 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Simon Fraser University, Burnaby, British Columbia V5A 1S6, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25855291" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Conservation of Natural Resources/*methods/*trends ; *Coral Reefs ; *Ecosystem ; Fisheries/*methods/*statistics & numerical data ; Fishes/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 100
    Publication Date: 2015-09-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cord, Anna F -- Seppelt, Ralf -- Turner, Woody -- England -- Nature. 2015 Sep 3;525(7567):33. doi: 10.1038/525033a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Helmholtz Centre for Environmental Research (UFZ), Leipzig, Germany. ; NASA, Washington DC, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26333459" target="_blank"〉PubMed〈/a〉
    Keywords: Biodiversity ; Biofuels/supply & distribution ; Conservation of Natural Resources/*statistics & numerical data ; Ecology/*methods ; *Ecosystem ; Environmental Monitoring/instrumentation/*methods ; *Goals ; *Spacecraft ; United Nations
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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