ALBERT

Description: The abundances of 92Nb and 146Sm in the early solar system are determined from meteoritic analysis, and their stellar production is attributed to the p process. We investigate if their origin from thermonuclear supernovae deriving from the explosion of white dwarfs with mass above the Chandrasekhar limit is in agreement...

Description: Harnessing chemosynthetic symbionts is a recurring evolutionary strategy. Eukaryotes from six phyla as well as one archaeon have acquired chemoautotrophic sulfur-oxidizing bacteria. In contrast to this broad host diversity, known bacterial partners apparently belong to two classes of bacteria—the Gamma- and Epsilonproteobacteria. Here, we characterize the intracellular endosymbionts of the mouthless catenulid flatworm genus Paracatenula as chemoautotrophic sulfur-oxidizing Alphaproteobacteria. The symbionts of Paracatenula galateia are provisionally classified as “Candidatus Riegeria galateiae” based on 16S ribosomal RNA sequencing confirmed by fluorescence in situ hybridization together with functional gene and sulfur metabolite evidence. 16S rRNA gene phylogenetic analysis shows that all 16 Paracatenula species examined harbor host species-specific intracellular Candidatus Riegeria bacteria that form a monophyletic group within the order Rhodospirillales. Comparing host and symbiont phylogenies reveals strict cocladogenesis and points to vertical transmission of the symbionts. Between 33% and 50% of the body volume of the various worm species is composed of bacterial symbionts, by far the highest proportion among all known endosymbiotic associations between bacteria and metazoans. This symbiosis, which likely originated more than 500 Mya during the early evolution of flatworms, is the oldest known animal–chemoautotrophic bacteria association. The distant phylogenetic position of the symbionts compared with other mutualistic or parasitic Alphaproteobacteria promises to illuminate the common genetic predispositions that have allowed several members of this class to successfully colonize eukaryote cells.

Description: Human immunodeficiency virus-type 1 (HIV-1) infection is characterized by a chronic state of immune hyperactivation in patients. Infection of human peripheral blood lymphocytes with HIV-1 in vitro resulted in increased interleukin-2 (IL-2) secretion in response to T cell activation via the CD3 and CD28 receptors. Expression of the HIV-1 transactivator Tat recapitulated this phenotype and was associated with increased IL-2 secretion in response to costimulation with CD3 plus CD28. IL-2 superinduction by Tat occurred at the transcriptional level, was mediated by the CD28-responsive element in the IL-2 promoter, and was exclusively dependent on the 29 amino acids encoded by the second exon of Tat.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ott, M -- Emiliani, S -- Van Lint, C -- Herbein, G -- Lovett, J -- Chirmule, N -- McCloskey, T -- Pahwa, S -- Verdin, E -- New York, N.Y. -- Science. 1997 Mar 7;275(5305):1481-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Picower Institute for Medical Research, 350 Community Drive, Manhasset, NY 11030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9045614" target="_blank"〉PubMed〈/a〉

Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Christensen, Soren Tvorup -- Ott, Carolyn Marie -- New York, N.Y. -- Science. 2007 Jul 20;317(5836):330-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, University of Copenhagen, Copenhagen DK-2100, Denmark. stchristensen@aki.ku.dk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17641189" target="_blank"〉PubMed〈/a〉

Description: Activation of the aryl hydrocarbon receptor (AHR) by environmental xenobiotic toxic chemicals, for instance 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin), has been implicated in a variety of cellular processes such as embryogenesis, transformation, tumorigenesis and inflammation. But the identity of an endogenous ligand activating the AHR under physiological conditions in the absence of environmental toxic chemicals is still unknown. Here we identify the tryptophan (Trp) catabolite kynurenine (Kyn) as an endogenous ligand of the human AHR that is constitutively generated by human tumour cells via tryptophan-2,3-dioxygenase (TDO), a liver- and neuron-derived Trp-degrading enzyme not yet implicated in cancer biology. TDO-derived Kyn suppresses antitumour immune responses and promotes tumour-cell survival and motility through the AHR in an autocrine/paracrine fashion. The TDO-AHR pathway is active in human brain tumours and is associated with malignant progression and poor survival. Because Kyn is produced during cancer progression and inflammation in the local microenvironment in amounts sufficient for activating the human AHR, these results provide evidence for a previously unidentified pathophysiological function of the AHR with profound implications for cancer and immune biology.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Opitz, Christiane A -- Litzenburger, Ulrike M -- Sahm, Felix -- Ott, Martina -- Tritschler, Isabel -- Trump, Saskia -- Schumacher, Theresa -- Jestaedt, Leonie -- Schrenk, Dieter -- Weller, Michael -- Jugold, Manfred -- Guillemin, Gilles J -- Miller, Christine L -- Lutz, Christian -- Radlwimmer, Bernhard -- Lehmann, Irina -- von Deimling, Andreas -- Wick, Wolfgang -- Platten, Michael -- England -- Nature. 2011 Oct 5;478(7368):197-203. doi: 10.1038/nature10491.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurooncology, Neurology Clinic and National Center for Tumor Diseases, University Hospital of Heidelberg, 69120 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21976023" target="_blank"〉PubMed〈/a〉

Description: Upon the aberrant activation of oncogenes, normal cells can enter the cellular senescence program, a state of stable cell-cycle arrest, which represents an important barrier against tumour development in vivo. Senescent cells communicate with their environment by secreting various cytokines and growth factors, and it was reported that this 'secretory phenotype' can have pro- as well as anti-tumorigenic effects. Here we show that oncogene-induced senescence occurs in otherwise normal murine hepatocytes in vivo. Pre-malignant senescent hepatocytes secrete chemo- and cytokines and are subject to immune-mediated clearance (designated as 'senescence surveillance'), which depends on an intact CD4(+) T-cell-mediated adaptive immune response. Impaired immune surveillance of pre-malignant senescent hepatocytes results in the development of murine hepatocellular carcinomas (HCCs), thus showing that senescence surveillance is important for tumour suppression in vivo. In accordance with these observations, ras-specific Th1 lymphocytes could be detected in mice, in which oncogene-induced senescence had been triggered by hepatic expression of Nras(G12V). We also found that CD4(+) T cells require monocytes/macrophages to execute the clearance of senescent hepatocytes. Our study indicates that senescence surveillance represents an important extrinsic component of the senescence anti-tumour barrier, and illustrates how the cellular senescence program is involved in tumour immune surveillance by mounting specific immune responses against antigens expressed in pre-malignant senescent cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kang, Tae-Won -- Yevsa, Tetyana -- Woller, Norman -- Hoenicke, Lisa -- Wuestefeld, Torsten -- Dauch, Daniel -- Hohmeyer, Anja -- Gereke, Marcus -- Rudalska, Ramona -- Potapova, Anna -- Iken, Marcus -- Vucur, Mihael -- Weiss, Siegfried -- Heikenwalder, Mathias -- Khan, Sadaf -- Gil, Jesus -- Bruder, Dunja -- Manns, Michael -- Schirmacher, Peter -- Tacke, Frank -- Ott, Michael -- Luedde, Tom -- Longerich, Thomas -- Kubicka, Stefan -- Zender, Lars -- MC_U120085810/Medical Research Council/United Kingdom -- England -- Nature. 2011 Nov 9;479(7374):547-51. doi: 10.1038/nature10599.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Helmholtz Centre for Infection Research, Inhoffenstrasse 7, 38124 Braunschweig, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22080947" target="_blank"〉PubMed〈/a〉

Description: Monoallelic point mutations of isocitrate dehydrogenase type 1 (IDH1) are an early and defining event in the development of a subgroup of gliomas and other types of tumour. They almost uniformly occur in the critical arginine residue (Arg 132) in the catalytic pocket, resulting in a neomorphic enzymatic function, production of the oncometabolite 2-hydroxyglutarate (2-HG), genomic hypermethylation, genetic instability and malignant transformation. More than 70% of diffuse grade II and grade III gliomas carry the most frequent mutation, IDH1(R132H) (ref. 3). From an immunological perspective, IDH1(R132H) represents a potential target for immunotherapy as it is a tumour-specific potential neoantigen with high uniformity and penetrance expressed in all tumour cells. Here we demonstrate that IDH1(R132H) contains an immunogenic epitope suitable for mutation-specific vaccination. Peptides encompassing the mutated region are presented on major histocompatibility complexes (MHC) class II and induce mutation-specific CD4(+) T-helper-1 (TH1) responses. CD4(+) TH1 cells and antibodies spontaneously occurring in patients with IDH1(R132H)-mutated gliomas specifically recognize IDH1(R132H). Peptide vaccination of mice devoid of mouse MHC and transgenic for human MHC class I and II with IDH1(R132H) p123-142 results in an effective MHC class II-restricted mutation-specific antitumour immune response and control of pre-established syngeneic IDH1(R132H)-expressing tumours in a CD4(+) T-cell-dependent manner. As IDH1(R132H) is present in all tumour cells of these slow-growing gliomas, a mutation-specific anti-IDH1(R132H) vaccine may represent a viable novel therapeutic strategy for IDH1(R132H)-mutated tumours.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schumacher, Theresa -- Bunse, Lukas -- Pusch, Stefan -- Sahm, Felix -- Wiestler, Benedikt -- Quandt, Jasmin -- Menn, Oliver -- Osswald, Matthias -- Oezen, Iris -- Ott, Martina -- Keil, Melanie -- Balss, Jorg -- Rauschenbach, Katharina -- Grabowska, Agnieszka K -- Vogler, Isabel -- Diekmann, Jan -- Trautwein, Nico -- Eichmuller, Stefan B -- Okun, Jurgen -- Stevanovic, Stefan -- Riemer, Angelika B -- Sahin, Ugur -- Friese, Manuel A -- Beckhove, Philipp -- von Deimling, Andreas -- Wick, Wolfgang -- Platten, Michael -- England -- Nature. 2014 Aug 21;512(7514):324-7. doi: 10.1038/nature13387. Epub 2014 Jun 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Neurooncology, University Hospital Heidelberg and National Center for Tumor Diseases, 69120 Heidelberg, Germany [2] German Cancer Consortium (DKTK) Clinical Cooperation Unit Neuroimmunology and Brain Tumor Immunology, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany [3]. ; 1] Department of Neuropathology, University Hospital Heidelberg and National Center for Tumor Diseases, 69120 Heidelberg, Germany [2] German Cancer Consortium (DKTK) Clinical Cooperation Unit Neuropathology, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany. ; 1] Department of Neurooncology, University Hospital Heidelberg and National Center for Tumor Diseases, 69120 Heidelberg, Germany [2] German Cancer Consortium (DKTK) Clinical Cooperation Unit Neurooncology, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany. ; Department of Translational Immunology, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany. ; Department of Neurooncology, University Hospital Heidelberg and National Center for Tumor Diseases, 69120 Heidelberg, Germany. ; 1] Department of Neurooncology, University Hospital Heidelberg and National Center for Tumor Diseases, 69120 Heidelberg, Germany [2] German Cancer Consortium (DKTK) Clinical Cooperation Unit Neuroimmunology and Brain Tumor Immunology, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany. ; 1] German Cancer Consortium (DKTK) Clinical Cooperation Unit Neuroimmunology and Brain Tumor Immunology, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany [2] German Cancer Consortium (DKTK) Clinical Cooperation Unit Neuropathology, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany. ; Department of Immunotherapy and -prevention Group, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany. ; Ribological GmbH, 55131 Mainz, Germany. ; Translational Oncology, 55131 Mainz, Germany. ; Department of Immunology, University of Tubingen, 72076 Tubingen, Germany. ; Metabolic Centre Heidelberg, University Children's Hospital, 69120 Heidelberg, Germany. ; Center for Molecular Neurobiology, University Medical Center, Hamburg-Eppendorf, 20251 Hamburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25043048" target="_blank"〉PubMed〈/a〉

Description: In eukaryotes, post-translational modification of histones is critical for regulation of chromatin structure and gene expression. EZH2 is the catalytic subunit of the polycomb repressive complex 2 (PRC2) and is involved in repressing gene expression through methylation of histone H3 on lysine 27 (H3K27). EZH2 overexpression is implicated in tumorigenesis and correlates with poor prognosis in several tumour types. Additionally, somatic heterozygous mutations of Y641 and A677 residues within the catalytic SET domain of EZH2 occur in diffuse large B-cell lymphoma (DLBCL) and follicular lymphoma. The Y641 residue is the most frequently mutated residue, with up to 22% of germinal centre B-cell DLBCL and follicular lymphoma harbouring mutations at this site. These lymphomas have increased H3K27 tri-methylation (H3K27me3) owing to altered substrate preferences of the mutant enzymes. However, it is unknown whether specific, direct inhibition of EZH2 methyltransferase activity will be effective in treating EZH2 mutant lymphomas. Here we demonstrate that GSK126, a potent, highly selective, S-adenosyl-methionine-competitive, small-molecule inhibitor of EZH2 methyltransferase activity, decreases global H3K27me3 levels and reactivates silenced PRC2 target genes. GSK126 effectively inhibits the proliferation of EZH2 mutant DLBCL cell lines and markedly inhibits the growth of EZH2 mutant DLBCL xenografts in mice. Together, these data demonstrate that pharmacological inhibition of EZH2 activity may provide a promising treatment for EZH2 mutant lymphoma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McCabe, Michael T -- Ott, Heidi M -- Ganji, Gopinath -- Korenchuk, Susan -- Thompson, Christine -- Van Aller, Glenn S -- Liu, Yan -- Graves, Alan P -- Della Pietra, Anthony 3rd -- Diaz, Elsie -- LaFrance, Louis V -- Mellinger, Mark -- Duquenne, Celine -- Tian, Xinrong -- Kruger, Ryan G -- McHugh, Charles F -- Brandt, Martin -- Miller, William H -- Dhanak, Dashyant -- Verma, Sharad K -- Tummino, Peter J -- Creasy, Caretha L -- England -- Nature. 2012 Dec 6;492(7427):108-12. doi: 10.1038/nature11606. Epub 2012 Oct 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Epigenetics Discovery Performance Unit, Cancer Research, Oncology R&D, GlaxoSmithKline, 1250 S. Collegeville Road, Collegeville, Pennsylvania 19426, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23051747" target="_blank"〉PubMed〈/a〉

Description: Insects are the most speciose group of animals, but the phylogenetic relationships of many major lineages remain unresolved. We inferred the phylogeny of insects from 1478 protein-coding genes. Phylogenomic analyses of nucleotide and amino acid sequences, with site-specific nucleotide or domain-specific amino acid substitution models, produced statistically robust and congruent results resolving previously controversial phylogenetic relations hips. We dated the origin of insects to the Early Ordovician [~479 million years ago (Ma)], of insect flight to the Early Devonian (~406 Ma), of major extant lineages to the Mississippian (~345 Ma), and the major diversification of holometabolous insects to the Early Cretaceous. Our phylogenomic study provides a comprehensive reliable scaffold for future comparative analyses of evolutionary innovations among insects.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Misof, Bernhard -- Liu, Shanlin -- Meusemann, Karen -- Peters, Ralph S -- Donath, Alexander -- Mayer, Christoph -- Frandsen, Paul B -- Ware, Jessica -- Flouri, Tomas -- Beutel, Rolf G -- Niehuis, Oliver -- Petersen, Malte -- Izquierdo-Carrasco, Fernando -- Wappler, Torsten -- Rust, Jes -- Aberer, Andre J -- Aspock, Ulrike -- Aspock, Horst -- Bartel, Daniela -- Blanke, Alexander -- Berger, Simon -- Bohm, Alexander -- Buckley, Thomas R -- Calcott, Brett -- Chen, Junqing -- Friedrich, Frank -- Fukui, Makiko -- Fujita, Mari -- Greve, Carola -- Grobe, Peter -- Gu, Shengchang -- Huang, Ying -- Jermiin, Lars S -- Kawahara, Akito Y -- Krogmann, Lars -- Kubiak, Martin -- Lanfear, Robert -- Letsch, Harald -- Li, Yiyuan -- Li, Zhenyu -- Li, Jiguang -- Lu, Haorong -- Machida, Ryuichiro -- Mashimo, Yuta -- Kapli, Pashalia -- McKenna, Duane D -- Meng, Guanliang -- Nakagaki, Yasutaka -- Navarrete-Heredia, Jose Luis -- Ott, Michael -- Ou, Yanxiang -- Pass, Gunther -- Podsiadlowski, Lars -- Pohl, Hans -- von Reumont, Bjorn M -- Schutte, Kai -- Sekiya, Kaoru -- Shimizu, Shota -- Slipinski, Adam -- Stamatakis, Alexandros -- Song, Wenhui -- Su, Xu -- Szucsich, Nikolaus U -- Tan, Meihua -- Tan, Xuemei -- Tang, Min -- Tang, Jingbo -- Timelthaler, Gerald -- Tomizuka, Shigekazu -- Trautwein, Michelle -- Tong, Xiaoli -- Uchifune, Toshiki -- Walzl, Manfred G -- Wiegmann, Brian M -- Wilbrandt, Jeanne -- Wipfler, Benjamin -- Wong, Thomas K F -- Wu, Qiong -- Wu, Gengxiong -- Xie, Yinlong -- Yang, Shenzhou -- Yang, Qing -- Yeates, David K -- Yoshizawa, Kazunori -- Zhang, Qing -- Zhang, Rui -- Zhang, Wenwei -- Zhang, Yunhui -- Zhao, Jing -- Zhou, Chengran -- Zhou, Lili -- Ziesmann, Tanja -- Zou, Shijie -- Li, Yingrui -- Xu, Xun -- Zhang, Yong -- Yang, Huanming -- Wang, Jian -- Wang, Jun -- Kjer, Karl M -- Zhou, Xin -- New York, N.Y. -- Science. 2014 Nov 7;346(6210):763-7. doi: 10.1126/science.1257570. Epub 2014 Nov 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Zoologisches Forschungsmuseum Alexander Koenig (ZFMK)/Zentrum fur Molekulare Biodiversitatsforschung (ZMB), Bonn, Germany. xinzhou@genomics.cn b.misof.zfmk@uni-bonn.de kjer@aesop.rutgers.edu wangj@genomics.cn. ; China National GeneBank, BGI-Shenzhen, China. BGI-Shenzhen, China. ; Zoologisches Forschungsmuseum Alexander Koenig (ZFMK)/Zentrum fur Molekulare Biodiversitatsforschung (ZMB), Bonn, Germany. Australian National Insect Collection, Commonwealth Scientific and Industrial Research Organization (Australia) (CSIRO), National Research Collections Australia, Canberra, ACT, Australia. ; Abteilung Arthropoda, Zoologisches Forschungsmuseum Alexander Koenig (ZFMK), Bonn, Germany. ; Zoologisches Forschungsmuseum Alexander Koenig (ZFMK)/Zentrum fur Molekulare Biodiversitatsforschung (ZMB), Bonn, Germany. ; Department of Entomology, Rutgers University, New Brunswick, NJ 08854, USA. ; Department of Biological Sciences, Rutgers University, Newark, NJ 08854, USA. ; Scientific Computing, Heidelberg Institute for Theoretical Studies (HITS), Heidelberg, Germany. ; Institut fur Spezielle Zoologie und Evolutionsbiologie mit Phyletischem Museum Jena, FSU Jena, Germany. ; Steinmann-Institut, Bereich Palaontologie, Universitat Bonn, Germany. ; 2. Zoologische Abteilung (Insekten), Naturhistorisches Museum Wien, Vienna, Austria. Department of Integrative Zoology, Universitat Wien, Vienna, Austria. ; Institut fur Spezifische Prophylaxe und Tropenmedizin, Medizinische Parasitologie, Medizinische Universitat Wien (MUW), Vienna, Austria. ; Department of Integrative Zoology, Universitat Wien, Vienna, Austria. ; Zoologisches Forschungsmuseum Alexander Koenig (ZFMK)/Zentrum fur Molekulare Biodiversitatsforschung (ZMB), Bonn, Germany. Sugadaira Montane Research Center/Hexapod Comparative Embryology Laboratory, University of Tsukuba, Japan. ; Manaaki Whenua Landcare Research, Auckland, New Zealand. ; Center for Advanced Modeling, Emergency Medicine Department, Johns Hopkins University, Baltimore, MD 21209, USA. ; BGI-Shenzhen, China. ; Biozentrum Grindel und Zoologisches Museum, Universitat Hamburg, Hamburg, Germany. ; Evolutionary Morphology Laboratory, Graduate School of Science and Engineering, Ehime University, Japan. ; Sugadaira Montane Research Center/Hexapod Comparative Embryology Laboratory, University of Tsukuba, Japan. ; Land and Water Flagship, CSIRO, Canberra, ACT, Australia. ; Florida Museum of Natural History, University of Florida, Gainesville, FL 32611, USA. ; Entomology, Staatliches Museum fur Naturkunde Stuttgart (SMNS), Germany. ; Ecology Evolution and Genetics, Research School of Biology, Australian National University, Canberra, ACT, Australia. National Evolutionary Synthesis Center, Durham, NC 27705, USA. Department of Biological Sciences, Macquarie University, Sydney, Australia. ; Department fur Botanik und Biodiversitatsforschung, Universitat Wien, Vienna, Austria. ; Scientific Computing, Heidelberg Institute for Theoretical Studies (HITS), Heidelberg, Germany. Natural History Museum of Crete, University of Crete, Post Office Box 2208, Gr-71409, Iraklio, and Biology Department, University of Crete, Iraklio, Crete, Greece. ; Department of Biological Sciences and Feinstone Center for Genomic Research, University of Memphis, Memphis, TN 38152, USA. ; Centro Universitario de Ciencias Biologicas y Agropecuarias, Centro de Estudios en Zoologia, Universidad de Guadalajara, Zapopan, Jalisco, Mexico. ; Leibniz Supercomputing Centre of the Bavarian Academy of Sciences and Humanities, Garching, Germany. ; Institute of Evolutionary Biology and Ecology, Zoology and Evolutionary Biology, University of Bonn, Bonn, Germany. ; Department of Life Sciences, The Natural History Museum London, London, UK. ; Abteilung Entomologie, Biozentrum Grindel und Zoologisches Museum, Universitat Hamburg, Hamburg, Germany. ; Australian National Insect Collection, Commonwealth Scientific and Industrial Research Organization (Australia) (CSIRO), National Research Collections Australia, Canberra, ACT, Australia. ; Scientific Computing, Heidelberg Institute for Theoretical Studies (HITS), Heidelberg, Germany. Fakultat fur Informatik, Karlsruher Institut fur Technologie, Karlsruhe, Germany. ; California Academy of Sciences, San Francisco, CA 94118, USA. ; Department of Entomology, College of Natural Resources and Environment, South China Agricultural University, China. ; Sugadaira Montane Research Center/Hexapod Comparative Embryology Laboratory, University of Tsukuba, Japan. Yokosuka City Museum, Yokosuka, Kanagawa, Japan. ; Department of Entomology, North Carolina State University, Raleigh, NC 27695, USA. ; Systematic Entomology, Hokkaido University, Sapporo, Japan. ; BGI-Shenzhen, China. Department of Biology, University of Copenhagen, Copenhagen, Denmark. Princess Al Jawhara Center of Excellence in the Research of Hereditary Disorders, King Abdulaziz University, Jeddah, Saudi Arabia. Macau University of Science and Technology, Avenida Wai Long, Taipa, Macau, China. Department of Medicine, University of Hong Kong, Hong Kong. xinzhou@genomics.cn b.misof.zfmk@uni-bonn.de kjer@aesop.rutgers.edu wangj@genomics.cn. ; Department of Ecology, Evolution, and Natural Resources, Rutgers University, New Brunswick, NJ 08854, USA. xinzhou@genomics.cn b.misof.zfmk@uni-bonn.de kjer@aesop.rutgers.edu wangj@genomics.cn. ; China National GeneBank, BGI-Shenzhen, China. BGI-Shenzhen, China. xinzhou@genomics.cn b.misof.zfmk@uni-bonn.de kjer@aesop.rutgers.edu wangj@genomics.cn.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25378627" target="_blank"〉PubMed〈/a〉

Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ott, Martin -- England -- Nature. 2016 May 11;533(7604):472-3. doi: 10.1038/nature18436.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Biomembrane Research, Department of Biochemistry and Biophysics, Stockholm University, SE-106 91 Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27225113" target="_blank"〉PubMed〈/a〉