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  • Male  (1,272)
  • Mutation  (588)
  • Signal Transduction  (332)
  • American Association for the Advancement of Science (AAAS)  (2,057)
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  • 1
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-03-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gregersen, Peter K -- New York, N.Y. -- Science. 2014 Mar 7;343(6175):1087-8. doi: 10.1126/science.1251426.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Robert S. Boas Center for Genomics and Human Genetics, The Feinstein Institute for Medical Research, North Shore LIJ Health System, 350 Community Drive, Manhasset, NY 110430, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24604188" target="_blank"〉PubMed〈/a〉
    Keywords: Crohn Disease/*genetics ; Dendritic Cells/*immunology ; Female ; Gene Expression Regulation/*immunology ; *Gene-Environment Interaction ; *Genetic Predisposition to Disease ; Host-Pathogen Interactions/*genetics ; Humans ; Immunity, Innate/*genetics ; Interferon Regulatory Factor-7/*genetics ; Male ; Monocytes/*immunology ; STAT Transcription Factors/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2014-05-17
    Description: A switchlike response in nuclear factor-kappaB (NF-kappaB) activity implies the existence of a threshold in the NF-kappaB signaling module. We show that the CARD-containing MAGUK protein 1 (CARMA1, also called CARD11)-TAK1 (MAP3K7)-inhibitor of NF-kappaB (IkappaB) kinase-beta (IKKbeta) module is a switch mechanism for NF-kappaB activation in B cell receptor (BCR) signaling. Experimental and mathematical modeling analyses showed that IKK activity is regulated by positive feedback from IKKbeta to TAK1, generating a steep dose response to BCR stimulation. Mutation of the scaffolding protein CARMA1 at serine-578, an IKKbeta target, abrogated not only late TAK1 activity, but also the switchlike activation of NF-kappaB in single cells, suggesting that phosphorylation of this residue accounts for the feedback.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shinohara, Hisaaki -- Behar, Marcelo -- Inoue, Kentaro -- Hiroshima, Michio -- Yasuda, Tomoharu -- Nagashima, Takeshi -- Kimura, Shuhei -- Sanjo, Hideki -- Maeda, Shiori -- Yumoto, Noriko -- Ki, Sewon -- Akira, Shizuo -- Sako, Yasushi -- Hoffmann, Alexander -- Kurosaki, Tomohiro -- Okada-Hatakeyama, Mariko -- 5R01CA141722/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2014 May 16;344(6185):760-4. doi: 10.1126/science.1250020.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Integrated Cellular Systems, RIKEN Center for Integrative Medical Sciences (IMS-RCAI), Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan. ; Signaling Systems Laboratory, Department of Chemistry and Biochemistry, University of California, San Diego, La Jolla, CA 92093, USA. Institute for Quantitative and Computational Biosciences (QC Bio) and Department of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, Los Angeles, CA 90025, USA. ; Laboratory for Cell Signaling Dynamics, RIKEN Quantitative Biology Center (QBiC), 6-2-3, Furuedai, Suita, Osaka 565-0874, Japan. Cellular Informatics Laboratory, RIKEN, 2-1 Hirosawa, Wako 351-0198, Japan. ; Laboratory for Lymphocyte Differentiation, RIKEN Center for Integrative Medical Sciences (IMS-RCAI), Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan. ; Graduate School of Engineering, Tottori University 4-101, Koyama-minami, Tottori 680-8552, Japan. ; Laboratory of Host Defense, WPI Immunology Frontier Research Center, Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan. ; Cellular Informatics Laboratory, RIKEN, 2-1 Hirosawa, Wako 351-0198, Japan. ; Signaling Systems Laboratory, Department of Chemistry and Biochemistry, University of California, San Diego, La Jolla, CA 92093, USA. Institute for Quantitative and Computational Biosciences (QC Bio) and Department of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, Los Angeles, CA 90025, USA. ahoffmann@ucla.edu kurosaki@rcai.riken.jp marikoh@rcai.riken.jp. ; Laboratory for Lymphocyte Differentiation, RIKEN Center for Integrative Medical Sciences (IMS-RCAI), Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan. Laboratory for Lymphocyte Differentiation, WPI Immunology Frontier Research Center, Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan. ahoffmann@ucla.edu kurosaki@rcai.riken.jp marikoh@rcai.riken.jp. ; Laboratory for Integrated Cellular Systems, RIKEN Center for Integrative Medical Sciences (IMS-RCAI), Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan. ahoffmann@ucla.edu kurosaki@rcai.riken.jp marikoh@rcai.riken.jp.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24833394" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/metabolism ; CARD Signaling Adaptor Proteins/genetics/*metabolism ; Cell Line ; Chickens ; Feedback, Physiological ; Guanylate Cyclase/genetics/*metabolism ; I-kappa B Kinase/*metabolism ; MAP Kinase Kinase Kinases/genetics/*metabolism ; Mice ; Mice, Knockout ; Mutation ; NF-kappa B/*agonists ; Phosphorylation ; Receptors, Antigen, B-Cell/genetics/*metabolism ; Serine/genetics/metabolism ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-10-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbons, Ann -- New York, N.Y. -- Science. 2014 Oct 24;346(6208):405-6. doi: 10.1126/science.346.6208.405.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25342776" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Domestic/*psychology ; *Biological Evolution ; *Cooperative Behavior ; Female ; Hominidae/anatomy & histology/psychology ; Humans ; Male ; Skull/*anatomy & histology ; Testosterone/metabolism ; Tooth/anatomy & histology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2014-09-23
    Description: The neuromuscular junction (NMJ) is the synapse between a motor neuron and skeletal muscle. Defects in NMJ transmission cause muscle weakness, termed myasthenia. The muscle protein Dok-7 is essential for activation of the receptor kinase MuSK, which governs NMJ formation, and DOK7 mutations underlie familial limb-girdle myasthenia (DOK7 myasthenia), a neuromuscular disease characterized by small NMJs. Here, we show in a mouse model of DOK7 myasthenia that therapeutic administration of an adeno-associated virus (AAV) vector encoding the human DOK7 gene resulted in an enlargement of NMJs and substantial increases in muscle strength and life span. When applied to model mice of another neuromuscular disorder, autosomal dominant Emery-Dreifuss muscular dystrophy, DOK7 gene therapy likewise resulted in enlargement of NMJs as well as positive effects on motor activity and life span. These results suggest that therapies aimed at enlarging the NMJ may be useful for a range of neuromuscular disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arimura, Sumimasa -- Okada, Takashi -- Tezuka, Tohru -- Chiyo, Tomoko -- Kasahara, Yuko -- Yoshimura, Toshiro -- Motomura, Masakatsu -- Yoshida, Nobuaki -- Beeson, David -- Takeda, Shin'ichi -- Yamanashi, Yuji -- G0701521/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2014 Sep 19;345(6203):1505-8. doi: 10.1126/science.1250744.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Genetics, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan. ; Department of Molecular Therapy, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan. ; Department of Occupational Therapy, Nagasaki University School of Health Sciences, Nagasaki, Japan. ; Department of Electrical and Electronics Engineering, Faculty of Engineering, Nagasaki Institute of Applied Science, Nagasaki, Japan. ; Laboratory of Developmental Genetics, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan. ; Neurosciences Group, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, UK. ; Division of Genetics, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan. yyamanas@ims.u-tokyo.ac.jp.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25237101" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dependovirus ; Disease Models, Animal ; Female ; Genetic Therapy/*methods ; Genetic Vectors/administration & dosage ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Muscle Proteins/*genetics ; Muscle, Skeletal/*innervation/physiopathology ; Muscular Dystrophies, Limb-Girdle/genetics/*pathology/*therapy ; Neuromuscular Junction/*pathology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2014-03-29
    Description: The field of optogenetics uses channelrhodopsins (ChRs) for light-induced neuronal activation. However, optimized tools for cellular inhibition at moderate light levels are lacking. We found that replacement of E90 in the central gate of ChR with positively charged residues produces chloride-conducting ChRs (ChloCs) with only negligible cation conductance. Molecular dynamics modeling unveiled that a high-affinity Cl(-)-binding site had been generated near the gate. Stabilizing the open state dramatically increased the operational light sensitivity of expressing cells (slow ChloC). In CA1 pyramidal cells, ChloCs completely inhibited action potentials triggered by depolarizing current injections or synaptic stimulation. Thus, by inverting the charge of the selectivity filter, we have created a class of directly light-gated anion channels that can be used to block neuronal output in a fully reversible fashion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wietek, Jonas -- Wiegert, J Simon -- Adeishvili, Nona -- Schneider, Franziska -- Watanabe, Hiroshi -- Tsunoda, Satoshi P -- Vogt, Arend -- Elstner, Marcus -- Oertner, Thomas G -- Hegemann, Peter -- New York, N.Y. -- Science. 2014 Apr 25;344(6182):409-12. doi: 10.1126/science.1249375. Epub 2014 Mar 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Biology, Experimental Biophysics, Humboldt Universitat zu Berlin, D-10115 Berlin, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24674867" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Binding Sites ; CA1 Region, Hippocampal/cytology ; Chloride Channels/*chemistry/*metabolism ; Chlorides/*metabolism ; HEK293 Cells ; Humans ; Hydrogen Bonding ; Ion Channel Gating ; Light ; Models, Molecular ; Molecular Dynamics Simulation ; Mutation ; Patch-Clamp Techniques ; Protein Conformation ; Protein Engineering ; Pyramidal Cells/metabolism ; Rats ; Recombinant Fusion Proteins/chemistry ; Rhodopsin/*chemistry/genetics/*metabolism ; Transfection
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 2014-10-04
    Description: After an infection, pathogen-specific tissue-resident memory T cells (T(RM) cells) persist in nonlymphoid tissues to provide rapid control upon reinfection, and vaccination strategies that create T(RM) cell pools at sites of pathogen entry are therefore attractive. However, it is not well understood how T(RM) cells provide such pathogen protection. Here, we demonstrate that activated T(RM) cells in mouse skin profoundly alter the local tissue environment by inducing a number of broadly active antiviral and antibacterial genes. This "pathogen alert" allows skin T(RM) cells to protect against an antigenically unrelated virus. These data describe a mechanism by which tissue-resident memory CD8(+) T cells protect previously infected sites that is rapid, amplifies the activation of a small number of cells into an organ-wide response, and has the capacity to control escape variants.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ariotti, Silvia -- Hogenbirk, Marc A -- Dijkgraaf, Feline E -- Visser, Lindy L -- Hoekstra, Mirjam E -- Song, Ji-Ying -- Jacobs, Heinz -- Haanen, John B -- Schumacher, Ton N -- New York, N.Y. -- Science. 2014 Oct 3;346(6205):101-5. doi: 10.1126/science.1254803. Epub 2014 Aug 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Immunology, Netherlands Cancer Institute, 1066 CX Amsterdam, Netherlands. ; Division of Biological Stress Response, Netherlands Cancer Institute, 1066 CX Amsterdam, Netherlands. ; Experimental Animal Pathology, Netherlands Cancer Institute, 1066 CX Amsterdam, Netherlands. ; Division of Immunology, Netherlands Cancer Institute, 1066 CX Amsterdam, Netherlands. t.schumacher@nki.nl.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25278612" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD8-Positive T-Lymphocytes/*immunology ; Female ; Immunologic Memory/genetics/*immunology ; Male ; Mice ; Skin/*immunology/microbiology/virology ; Transcriptome
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    Topics: Biology , Chemistry and Pharmacology , 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)
    Publication Date: 2014-04-05
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4143233/" 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/PMC4143233/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mann, Richard S -- R01 NS070644/NS/NINDS NIH HHS/ -- R01NS070644/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2014 Apr 4;344(6179):48-9. doi: 10.1126/science.1252431.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biophysics, Columbia University, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24700848" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Drosophila/*physiology ; Female ; Male ; Neurons/*physiology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-06-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbons, Ann -- New York, N.Y. -- Science. 2014 Jun 13;344(6189):1213-4. doi: 10.1126/science.344.6189.1213.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24925995" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Horses/*genetics/*physiology ; *Inbreeding ; Male ; *Physical Conditioning, Animal ; *Running ; Selection, Genetic
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-05-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Couzin-Frankel, Jennifer -- New York, N.Y. -- Science. 2014 May 23;344(6186):793-7. doi: 10.1126/science.344.6186.793.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24855236" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Antipsychotic Agents/therapeutic use ; *Bioethical Issues ; Conflict of Interest/*economics ; Dibenzothiazepines/therapeutic use ; Drug Industry/economics/ethics ; Ethicists/*psychology ; *Ethics, Medical ; Humans ; Male ; Minnesota ; Quetiapine Fumarate ; Randomized Controlled Trials as Topic/*ethics ; Schizophrenia/drug therapy ; Suicide/*ethics ; Truth Disclosure/*ethics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 2014-05-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Couzin-Frankel, Jennifer -- New York, N.Y. -- Science. 2014 May 16;344(6185):679. doi: 10.1126/science.344.6185.679.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24833367" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Experimentation/*standards ; Animals ; Biomedical Research/*standards ; Cells ; Female ; Male ; Mice ; National Institutes of Health (U.S.) ; Sex Factors ; United States ; X Chromosome ; Y Chromosome
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  • 11
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-02-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbons, Ann -- New York, N.Y. -- Science. 2014 Jan 31;343(6170):471-2. doi: 10.1126/science.343.6170.471.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24482455" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Crohn Disease/genetics ; DNA/genetics ; Diabetes Mellitus, Type 2/genetics ; Disease/*genetics ; *Evolution, Molecular ; Female ; Genome, Human/*genetics ; Humans ; Interleukin-18/genetics ; Keratins/genetics ; Liver Cirrhosis, Biliary/genetics ; Male ; Neanderthals/*genetics ; Optic Disk/anatomy & histology ; Sequence Analysis, DNA ; Smoking/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 12
    Publication Date: 2014-11-15
    Description: Activators of innate immunity may have the potential to combat a broad range of infectious agents. We report that treatment with bacterial flagellin prevented rotavirus (RV) infection in mice and cured chronically RV-infected mice. Protection was independent of adaptive immunity and interferon (IFN, type I and II) and required flagellin receptors Toll-like receptor 5 (TLR5) and NOD-like receptor C4 (NLRC4). Flagellin-induced activation of TLR5 on dendritic cells elicited production of the cytokine interleukin-22 (IL-22), which induced a protective gene expression program in intestinal epithelial cells. Flagellin also induced NLRC4-dependent production of IL-18 and immediate elimination of RV-infected cells. Administration of IL-22 and IL-18 to mice fully recapitulated the capacity of flagellin to prevent or eliminate RV infection and thus holds promise as a broad-spectrum antiviral agent.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Benyue -- Chassaing, Benoit -- Shi, Zhenda -- Uchiyama, Robin -- Zhang, Zhan -- Denning, Timothy L -- Crawford, Sue E -- Pruijssers, Andrea J -- Iskarpatyoti, Jason A -- Estes, Mary K -- Dermody, Terence S -- Ouyang, Wenjun -- Williams, Ifor R -- Vijay-Kumar, Matam -- Gewirtz, Andrew T -- AI038296/AI/NIAID NIH HHS/ -- AI080656/AI/NIAID NIH HHS/ -- AI107943/AI/NIAID NIH HHS/ -- DK061417/DK/NIDDK NIH HHS/ -- DK064730/DK/NIDDK NIH HHS/ -- DK56338/DK/NIDDK NIH HHS/ -- R01 AI038296/AI/NIAID NIH HHS/ -- R37 AI038296/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2014 Nov 14;346(6211):861-5. doi: 10.1126/science.1256999.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Inflammation, Immunity and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA, USA. ; Center for Inflammation, Immunity and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA, USA. Department of Pathology, Emory University School of Medicine, Atlanta, GA, USA. ; Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX, USA. ; Elizabeth B. Lamb Center for Pediatric Research, Vanderbilt University School of Medicine, Nashville, TN, USA. ; Elizabeth B. Lamb Center for Pediatric Research, Vanderbilt University School of Medicine, Nashville, TN, USA. Departments of Pediatrics, Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, TN, USA. ; Department of Immunology, Genentech, South San Francisco, CA, USA. ; Department of Pathology, Emory University School of Medicine, Atlanta, GA, USA. ; Department of Nutritional Sciences and Medicine, Pennsylvania State University, University Park, PA 16802, USA. ; Center for Inflammation, Immunity and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA, USA. Department of Pathology, Emory University School of Medicine, Atlanta, GA, USA. agewirtz@gsu.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25395539" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Diarrhea/immunology/therapy/virology ; Disease Models, Animal ; Feces/virology ; Flagellin/*administration & dosage/immunology ; Homeodomain Proteins/genetics ; *Immunity, Innate ; Interleukin-18/administration & dosage/genetics/*immunology ; Interleukins/administration & dosage/genetics/*immunology ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Mutation ; Rotavirus Infections/immunology/*prevention & control/therapy ; Toll-Like Receptor 5/genetics/*physiology ; Virus Shedding
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  • 13
    Publication Date: 2014-09-13
    Description: In its largest outbreak, Ebola virus disease is spreading through Guinea, Liberia, Sierra Leone, and Nigeria. We sequenced 99 Ebola virus genomes from 78 patients in Sierra Leone to ~2000x coverage. We observed a rapid accumulation of interhost and intrahost genetic variation, allowing us to characterize patterns of viral transmission over the initial weeks of the epidemic. This West African variant likely diverged from central African lineages around 2004, crossed from Guinea to Sierra Leone in May 2014, and has exhibited sustained human-to-human transmission subsequently, with no evidence of additional zoonotic sources. Because many of the mutations alter protein sequences and other biologically meaningful targets, they should be monitored for impact on diagnostics, vaccines, and therapies critical to outbreak response.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4431643/" 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/PMC4431643/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gire, Stephen K -- Goba, Augustine -- Andersen, Kristian G -- Sealfon, Rachel S G -- Park, Daniel J -- Kanneh, Lansana -- Jalloh, Simbirie -- Momoh, Mambu -- Fullah, Mohamed -- Dudas, Gytis -- Wohl, Shirlee -- Moses, Lina M -- Yozwiak, Nathan L -- Winnicki, Sarah -- Matranga, Christian B -- Malboeuf, Christine M -- Qu, James -- Gladden, Adrianne D -- Schaffner, Stephen F -- Yang, Xiao -- Jiang, Pan-Pan -- Nekoui, Mahan -- Colubri, Andres -- Coomber, Moinya Ruth -- Fonnie, Mbalu -- Moigboi, Alex -- Gbakie, Michael -- Kamara, Fatima K -- Tucker, Veronica -- Konuwa, Edwin -- Saffa, Sidiki -- Sellu, Josephine -- Jalloh, Abdul Azziz -- Kovoma, Alice -- Koninga, James -- Mustapha, Ibrahim -- Kargbo, Kandeh -- Foday, Momoh -- Yillah, Mohamed -- Kanneh, Franklyn -- Robert, Willie -- Massally, James L B -- Chapman, Sinead B -- Bochicchio, James -- Murphy, Cheryl -- Nusbaum, Chad -- Young, Sarah -- Birren, Bruce W -- Grant, Donald S -- Scheiffelin, John S -- Lander, Eric S -- Happi, Christian -- Gevao, Sahr M -- Gnirke, Andreas -- Rambaut, Andrew -- Garry, Robert F -- Khan, S Humarr -- Sabeti, Pardis C -- 095831/Wellcome Trust/United Kingdom -- 1DP2OD006514-01/OD/NIH HHS/ -- 1U01HG007480-01/HG/NHGRI NIH HHS/ -- 260864/European Research Council/International -- DP2 OD006514/OD/NIH HHS/ -- GM080177/GM/NIGMS NIH HHS/ -- HHSN272200900049C/AI/NIAID NIH HHS/ -- HHSN272200900049C/PHS HHS/ -- T32 GM080177/GM/NIGMS NIH HHS/ -- U01 HG007480/HG/NHGRI NIH HHS/ -- U19 AI110818/AI/NIAID NIH HHS/ -- U19 AI115589/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2014 Sep 12;345(6202):1369-72. doi: 10.1126/science.1259657. Epub 2014 Aug 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Systems Biology, Department of Organismic and Evolutionary Biology, Harvard University, Cambridge, MA 02138, USA. Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. ; Kenema Government Hospital, Kenema, Sierra Leone. andersen@broadinstitute.org augstgoba@yahoo.com psabeti@oeb.harvard.edu. ; Center for Systems Biology, Department of Organismic and Evolutionary Biology, Harvard University, Cambridge, MA 02138, USA. Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. andersen@broadinstitute.org augstgoba@yahoo.com psabeti@oeb.harvard.edu. ; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Computer Science and Artificial Intelligence Laboratory, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. ; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. ; Kenema Government Hospital, Kenema, Sierra Leone. ; Kenema Government Hospital, Kenema, Sierra Leone. Eastern Polytechnic College, Kenema, Sierra Leone. ; Institute of Evolutionary Biology, University of Edinburgh, Edinburgh EH9 3JT, UK. ; Center for Systems Biology, Department of Organismic and Evolutionary Biology, Harvard University, Cambridge, MA 02138, USA. Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Systems Biology, Harvard Medical School, Boston, MA 02115, USA. ; Tulane University Medical Center, New Orleans, LA 70112, USA. ; Center for Systems Biology, Department of Organismic and Evolutionary Biology, Harvard University, Cambridge, MA 02138, USA. ; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Systems Biology, Harvard Medical School, Boston, MA 02115, USA. Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. ; Redeemer's University, Ogun State, Nigeria. ; University of Sierra Leone, Freetown, Sierra Leone. ; Institute of Evolutionary Biology, University of Edinburgh, Edinburgh EH9 3JT, UK. Fogarty International Center, National Institutes of Health, Bethesda, MD 20892, USA. Centre for Immunity, Infection and Evolution, University of Edinburgh, Edinburgh EH9 3JT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25214632" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; *Disease Outbreaks ; Ebolavirus/*genetics/isolation & purification ; *Epidemiological Monitoring ; Genetic Variation ; Genome, Viral/genetics ; Genomics/methods ; Hemorrhagic Fever, Ebola/epidemiology/*transmission/*virology ; Humans ; Mutation ; Sequence Analysis, DNA ; Sierra Leone/epidemiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 14
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-10-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, Elizabeth -- New York, N.Y. -- Science. 2014 Oct 17;346(6207):292-5. doi: 10.1126/science.346.6207.292.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25324367" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Child ; Female ; Health ; Humans ; Infant ; Longevity ; Male ; Papio/*physiology/*psychology ; Reproduction ; Starvation/epidemiology/physiopathology ; Stress, Psychological/epidemiology/*physiopathology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 15
    Publication Date: 2014-12-17
    Description: Birds are the most species-rich class of tetrapod vertebrates and have wide relevance across many research fields. We explored bird macroevolution using full genomes from 48 avian species representing all major extant clades. The avian genome is principally characterized by its constrained size, which predominantly arose because of lineage-specific erosion of repetitive elements, large segmental deletions, and gene loss. Avian genomes furthermore show a remarkably high degree of evolutionary stasis at the levels of nucleotide sequence, gene synteny, and chromosomal structure. Despite this pattern of conservation, we detected many non-neutral evolutionary changes in protein-coding genes and noncoding regions. These analyses reveal that pan-avian genomic diversity covaries with adaptations to different lifestyles and convergent evolution of traits.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4390078/" 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/PMC4390078/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Guojie -- Li, Cai -- Li, Qiye -- Li, Bo -- Larkin, Denis M -- Lee, Chul -- Storz, Jay F -- Antunes, Agostinho -- Greenwold, Matthew J -- Meredith, Robert W -- Odeen, Anders -- Cui, Jie -- Zhou, Qi -- Xu, Luohao -- Pan, Hailin -- Wang, Zongji -- Jin, Lijun -- Zhang, Pei -- Hu, Haofu -- Yang, Wei -- Hu, Jiang -- Xiao, Jin -- Yang, Zhikai -- Liu, Yang -- Xie, Qiaolin -- Yu, Hao -- Lian, Jinmin -- Wen, Ping -- Zhang, Fang -- Li, Hui -- Zeng, Yongli -- Xiong, Zijun -- Liu, Shiping -- Zhou, Long -- Huang, Zhiyong -- An, Na -- Wang, Jie -- Zheng, Qiumei -- Xiong, Yingqi -- Wang, Guangbiao -- Wang, Bo -- Wang, Jingjing -- Fan, Yu -- da Fonseca, Rute R -- Alfaro-Nunez, Alonzo -- Schubert, Mikkel -- Orlando, Ludovic -- Mourier, Tobias -- Howard, Jason T -- Ganapathy, Ganeshkumar -- Pfenning, Andreas -- Whitney, Osceola -- Rivas, Miriam V -- Hara, Erina -- Smith, Julia -- Farre, Marta -- Narayan, Jitendra -- Slavov, Gancho -- Romanov, Michael N -- Borges, Rui -- Machado, Joao Paulo -- Khan, Imran -- Springer, Mark S -- Gatesy, John -- Hoffmann, Federico G -- Opazo, Juan C -- Hastad, Olle -- Sawyer, Roger H -- Kim, Heebal -- Kim, Kyu-Won -- Kim, Hyeon Jeong -- Cho, Seoae -- Li, Ning -- Huang, Yinhua -- Bruford, Michael W -- Zhan, Xiangjiang -- Dixon, Andrew -- Bertelsen, Mads F -- Derryberry, Elizabeth -- Warren, Wesley -- Wilson, Richard K -- Li, Shengbin -- Ray, David A -- Green, Richard E -- O'Brien, Stephen J -- Griffin, Darren -- Johnson, Warren E -- Haussler, David -- Ryder, Oliver A -- Willerslev, Eske -- Graves, Gary R -- Alstrom, Per -- Fjeldsa, Jon -- Mindell, David P -- Edwards, Scott V -- Braun, Edward L -- Rahbek, Carsten -- Burt, David W -- Houde, Peter -- Zhang, Yong -- Yang, Huanming -- Wang, Jian -- Avian Genome Consortium -- Jarvis, Erich D -- Gilbert, M Thomas P -- Wang, Jun -- DP1 OD000448/OD/NIH HHS/ -- DP1OD000448/OD/NIH HHS/ -- R01 HL087216/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Dec 12;346(6215):1311-20. doi: 10.1126/science.1251385. Epub 2014 Dec 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉China National GeneBank, Beijing Genomics Institute (BGI)-Shenzhen, Shenzhen, 518083, China. Centre for Social Evolution, Department of Biology, Universitetsparken 15, University of Copenhagen, DK-2100 Copenhagen, Denmark. zhanggj@genomics.cn jarvis@neuro.duke.edu mtpgilbert@gmail.com wangj@genomics.cn. ; China National GeneBank, Beijing Genomics Institute (BGI)-Shenzhen, Shenzhen, 518083, China. Centre for GeoGenetics, Natural History Museum of Denmark, University of Copenhagen, Oster Voldgade 5-7, 1350 Copenhagen, Denmark. ; China National GeneBank, Beijing Genomics Institute (BGI)-Shenzhen, Shenzhen, 518083, China. ; Royal Veterinary College, University of London, London, UK. ; Interdisciplinary Program in Bioinformatics, Seoul National University, Seoul 151-742, Republic of Korea. Cho and Kim Genomics, Seoul National University Research Park, Seoul 151-919, Republic of Korea. ; School of Biological Sciences, University of Nebraska, Lincoln, NE 68588, USA. ; Centro de Investigacion en Ciencias del Mar y Limnologia (CIMAR)/Centro Interdisciplinar de Investigacao Marinha e Ambiental (CIIMAR), Universidade do Porto, Rua dos Bragas, 177, 4050-123 Porto, Portugal. Departamento de Biologia, Faculdade de Ciencias, Universidade do Porto, Rua do Campo Alegre, 4169-007 Porto, Portugal. ; Department of Biological Sciences, University of South Carolina, Columbia, SC, USA. ; Department of Biology and Molecular Biology, Montclair State University, Montclair, NJ 07043, USA. ; Department of Animal Ecology, Uppsala University, Norbyvagen 18D, S-752 36 Uppsala, Sweden. ; Marie Bashir Institute for Infectious Diseases and Biosecurity, Charles Perkins Centre, School of Biological Sciences and Sydney Medical School, The University of Sydney, Sydney, NSW 2006, Australia. Program in Emerging Infectious Diseases, Duke-NUS Graduate Medical School, Singapore 169857, Singapore. ; Department of Integrative Biology University of California, Berkeley, CA 94720, USA. ; China National GeneBank, Beijing Genomics Institute (BGI)-Shenzhen, Shenzhen, 518083, China. College of Life Sciences, Wuhan University, Wuhan 430072, China. ; China National GeneBank, Beijing Genomics Institute (BGI)-Shenzhen, Shenzhen, 518083, China. School of Bioscience and Bioengineering, South China University of Technology, Guangzhou 510006, China. ; China National GeneBank, Beijing Genomics Institute (BGI)-Shenzhen, Shenzhen, 518083, China. BGI Education Center,University of Chinese Academy of Sciences,Shenzhen, 518083, China. ; Key Laboratory of Animal Models and Human Disease Mechanisms of Chinese Academy of Sciences and Yunnan Province, Kunming Institute of Zoology, Kunming, Yunnan 650223, China. ; Centre for GeoGenetics, Natural History Museum of Denmark, University of Copenhagen, Oster Voldgade 5-7, 1350 Copenhagen, Denmark. ; Department of Neurobiology, Howard Hughes Medical Institute, Duke University Medical Center, Durham, NC 27710, USA. ; Institute of Biological, Environmental and Rural Sciences, Aberystwyth University, Aberystwyth, UK. ; School of Biosciences, University of Kent, Canterbury CT2 7NJ, UK. ; Centro de Investigacion en Ciencias del Mar y Limnologia (CIMAR)/Centro Interdisciplinar de Investigacao Marinha e Ambiental (CIIMAR), Universidade do Porto, Rua dos Bragas, 177, 4050-123 Porto, Portugal. Instituto de Ciencias Biomedicas Abel Salazar (ICBAS), Universidade do Porto, Portugal. ; Department of Biology, University of California Riverside, Riverside, CA 92521, USA. ; Department of Biochemistry, Molecular Biology, Entomology and Plant Pathology, Mississippi State University, Mississippi State, MS 39762, USA. Institute for Genomics, Biocomputing and Biotechnology, Mississippi State University, Mississippi State, MS 39762, USA. ; Instituto de Ciencias Ambientales y Evolutivas, Facultad de Ciencias, Universidad Austral de Chile, Valdivia, Chile. ; Department of Anatomy, Physiology and Biochemistry, Swedish University of Agricultural Sciences, Post Office Box 7011, S-750 07, Uppsala, Sweden. ; Interdisciplinary Program in Bioinformatics, Seoul National University, Seoul 151-742, Republic of Korea. Cho and Kim Genomics, Seoul National University Research Park, Seoul 151-919, Republic of Korea. Department of Agricultural Biotechnology and Research Institute for Agriculture and Life Sciences, Seoul National University, Seoul 151-742, Republic of Korea. ; Interdisciplinary Program in Bioinformatics, Seoul National University, Seoul 151-742, Republic of Korea. ; Cho and Kim Genomics, Seoul National University Research Park, Seoul 151-919, Republic of Korea. ; State Key Laboratory for Agrobiotechnology, China Agricultural University, Beijing 100094, China. ; State Key Laboratory for Agrobiotechnology, China Agricultural University, Beijing 100094, China. College of Animal Science and Technology, China Agricultural University, Beijing 100094, China. ; Organisms and Environment Division, Cardiff School of Biosciences, Cardiff University, Cardiff CF10 3AX, Wales, UK. ; Organisms and Environment Division, Cardiff School of Biosciences, Cardiff University, Cardiff CF10 3AX, Wales, UK. Key Lab of Animal Ecology and Conservation Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101 China. ; International Wildlife Consultants, Carmarthen SA33 5YL, Wales, UK. ; Centre for Zoo and Wild Animal Health, Copenhagen Zoo, Roskildevej 38, DK-2000 Frederiksberg, Denmark. ; Department of Ecology and Evolutionary Biology, Tulane University, New Orleans, LA, USA. Museum of Natural Science, Louisiana State University, Baton Rouge, LA 70803, USA. ; The Genome Institute at Washington University, St. Louis, MO 63108, USA. ; College of Medicine and Forensics, Xi'an Jiaotong University, Xi'an, 710061, China. ; Institute for Genomics, Biocomputing and Biotechnology, Mississippi State University, Mississippi State, MS 39762, USA. ; Department of Biomolecular Engineering, University of California, Santa Cruz, CA 95064, USA. ; Theodosius Dobzhansky Center for Genome Bioinformatics, St. Petersburg State University, St. Petersburg, Russia. Nova Southeastern University Oceanographic Center 8000 N Ocean Drive, Dania, FL 33004, USA. ; Smithsonian Conservation Biology Institute, National Zoological Park, 1500 Remount Road, Front Royal, VA 22630, USA. ; Genetics Division, San Diego Zoo Institute for Conservation Research, 15600 San Pasqual Valley Road, Escondido, CA 92027, USA. ; Department of Vertebrate Zoology, MRC-116, National Museum of Natural History, Smithsonian Institution, Post Office Box 37012, Washington, DC 20013-7012, USA. Center for Macroecology, Evolution and Climate, the Natural History Museum of Denmark, University of Copenhagen, Universitetsparken 15, DK-2100 Copenhagen O, Denmark. ; Key Laboratory of Zoological Systematics and Evolution, Institute of Zoology, Chinese Academy of Sciences, 1 Beichen West Road, Chaoyang District, Beijing 100101, China. Swedish Species Information Centre, Swedish University of Agricultural Sciences, Box 7007, SE-750 07 Uppsala, Sweden. ; Center for Macroecology, Evolution and Climate, the Natural History Museum of Denmark, University of Copenhagen, Universitetsparken 15, DK-2100 Copenhagen O, Denmark. ; Department of Biochemistry & Biophysics, University of California, San Francisco, CA 94158, USA. ; Department of Organismic and Evolutionary Biology and Museum of Comparative Zoology, Harvard University, 26 Oxford Street, Cambridge, MA 02138, USA. ; Department of Biology and Genetics Institute, University of Florida, Gainesville, FL 32611, USA. ; Center for Macroecology, Evolution and Climate, the Natural History Museum of Denmark, University of Copenhagen, Universitetsparken 15, DK-2100 Copenhagen O, Denmark. Imperial College London, Grand Challenges in Ecosystems and the Environment Initiative, Silwood Park Campus, Ascot, Berkshire SL5 7PY, UK. ; Division of Genetics and Genomics, The Roslin Institute and Royal (Dick) School of Veterinary Studies, The Roslin Institute Building, University of Edinburgh, Easter Bush Campus, Midlothian EH25 9RG, UK. ; Department of Biology, New Mexico State University, Box 30001 MSC 3AF, Las Cruces, NM 88003, USA. ; China National GeneBank, Beijing Genomics Institute (BGI)-Shenzhen, Shenzhen, 518083, China. Macau University of Science and Technology, Avenida Wai long, Taipa, Macau 999078, China. ; Department of Neurobiology, Howard Hughes Medical Institute, Duke University Medical Center, Durham, NC 27710, USA. zhanggj@genomics.cn jarvis@neuro.duke.edu mtpgilbert@gmail.com wangj@genomics.cn. ; Centre for GeoGenetics, Natural History Museum of Denmark, University of Copenhagen, Oster Voldgade 5-7, 1350 Copenhagen, Denmark. Trace and Environmental DNA Laboratory, Department of Environment and Agriculture, Curtin University, Perth, Western Australia, 6102, Australia. zhanggj@genomics.cn jarvis@neuro.duke.edu mtpgilbert@gmail.com wangj@genomics.cn. ; China National GeneBank, Beijing Genomics Institute (BGI)-Shenzhen, Shenzhen, 518083, China. Macau University of Science and Technology, Avenida Wai long, Taipa, Macau 999078, China. Department of Biology, University of Copenhagen, Ole Maaloes Vej 5, 2200 Copenhagen, Denmark. Princess Al Jawhara Center of Excellence in the Research of Hereditary Disorders, King Abdulaziz University, Jeddah 21589, Saudi Arabia. Department of Medicine, University of Hong Kong, Hong Kong. zhanggj@genomics.cn jarvis@neuro.duke.edu mtpgilbert@gmail.com wangj@genomics.cn.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25504712" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; Animals ; Biodiversity ; *Biological Evolution ; Birds/classification/*genetics/physiology ; Conserved Sequence ; Diet ; *Evolution, Molecular ; Female ; Flight, Animal ; Genes ; Genetic Variation ; *Genome ; Genomics ; Male ; Molecular Sequence Annotation ; Phylogeny ; Reproduction/genetics ; Selection, Genetic ; Sequence Analysis, DNA ; Synteny ; Vision, Ocular/genetics ; Vocalization, Animal
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  • 16
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-11-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Augenlicht, Leonard -- New York, N.Y. -- Science. 2014 Nov 7;346(6210):710. doi: 10.1126/science.346.6210.710-a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Albert Einstein Cancer Center, Montefiore Medical Center, Department of Medicine and Cell Biology, Bronx, NY 10467, USA. leonard.augenlicht@einstein.yu.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25378612" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Combined Chemotherapy Protocols/*economics ; Brain Neoplasms/*drug therapy ; Drug Industry/*economics ; Humans ; Male ; *Mice ; Neoplasms, Experimental/*drug therapy ; Pancreatic Neoplasms/*drug therapy ; *Precision Medicine ; Sarcoma/*drug therapy ; *Xenograft Model Antitumor Assays
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  • 17
    Publication Date: 2014-11-15
    Description: DNA double-strand breaks (DSBs) are introduced in meiosis to initiate recombination and generate crossovers, the reciprocal exchanges of genetic material between parental chromosomes. Here, we present high-resolution maps of meiotic DSBs in individual human genomes. Comparing DSB maps between individuals shows that along with DNA binding by PRDM9, additional factors may dictate the efficiency of DSB formation. We find evidence for both GC-biased gene conversion and mutagenesis around meiotic DSB hotspots, while frequent colocalization of DSB hotspots with chromosome rearrangement breakpoints implicates the aberrant repair of meiotic DSBs in genomic disorders. Furthermore, our data indicate that DSB frequency is a major determinant of crossover rate. These maps provide new insights into the regulation of meiotic recombination and the impact of meiotic recombination on genome function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pratto, Florencia -- Brick, Kevin -- Khil, Pavel -- Smagulova, Fatima -- Petukhova, Galina V -- Camerini-Otero, R Daniel -- 1R01GM084104-01A1/GM/NIGMS NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2014 Nov 14;346(6211):1256442. doi: 10.1126/science.1256442.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Institute of Diabetes, Digestive and Kidney Diseases, NIH, Bethesda, MD, USA. ; Department of Biochemistry and Molecular Biology, Uniformed Services University of Health Sciences, Bethesda, MD, USA. ; Department of Biochemistry and Molecular Biology, Uniformed Services University of Health Sciences, Bethesda, MD, USA. rdcamerini@mail.nih.gov galina.petukhova@usuhs.edu. ; National Institute of Diabetes, Digestive and Kidney Diseases, NIH, Bethesda, MD, USA. rdcamerini@mail.nih.gov galina.petukhova@usuhs.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25395542" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; *Chromosome Mapping ; *DNA Breaks, Double-Stranded ; Genome, Human/*genetics ; *Genomic Instability ; Histone-Lysine N-Methyltransferase/genetics/metabolism ; *Homologous Recombination ; Humans ; Male ; Meiosis/*genetics ; Protein Binding ; Spermatocytes ; Telomere/genetics
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  • 18
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-07-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stone, Richard -- New York, N.Y. -- Science. 2014 Jul 11;345(6193):130-1, 133. doi: 10.1126/science.345.6193.130.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25013042" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Communicable Diseases, Emerging/*epidemiology/*prevention & control ; Encephalitis Viruses, Tick-Borne/isolation & purification ; Female ; Haplorhini ; Humans ; India/epidemiology ; Kyasanur Forest Disease/*epidemiology/*prevention & control ; Male ; Ticks/virology ; Trees
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  • 19
    Publication Date: 2014-10-11
    Description: Cancers are composed of populations of cells with distinct molecular and phenotypic features, a phenomenon termed intratumor heterogeneity (ITH). ITH in lung cancers has not been well studied. We applied multiregion whole-exome sequencing (WES) on 11 localized lung adenocarcinomas. All tumors showed clear evidence of ITH. On average, 76% of all mutations and 20 out of 21 known cancer gene mutations were identified in all regions of individual tumors, which suggested that single-region sequencing may be adequate to identify the majority of known cancer gene mutations in localized lung adenocarcinomas. With a median follow-up of 21 months after surgery, three patients have relapsed, and all three patients had significantly larger fractions of subclonal mutations in their primary tumors than patients without relapse. These data indicate that a larger subclonal mutation fraction may be associated with increased likelihood of postsurgical relapse in patients with localized lung adenocarcinomas.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4354858/" 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/PMC4354858/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Jianjun -- Fujimoto, Junya -- Zhang, Jianhua -- Wedge, David C -- Song, Xingzhi -- Zhang, Jiexin -- Seth, Sahil -- Chow, Chi-Wan -- Cao, Yu -- Gumbs, Curtis -- Gold, Kathryn A -- Kalhor, Neda -- Little, Latasha -- Mahadeshwar, Harshad -- Moran, Cesar -- Protopopov, Alexei -- Sun, Huandong -- Tang, Jiabin -- Wu, Xifeng -- Ye, Yuanqing -- William, William N -- Lee, J Jack -- Heymach, John V -- Hong, Waun Ki -- Swisher, Stephen -- Wistuba, Ignacio I -- Futreal, P Andrew -- CA016672/CA/NCI NIH HHS/ -- P30 CA016672/CA/NCI NIH HHS/ -- P50 CA070907/CA/NCI NIH HHS/ -- P50CA70907/CA/NCI NIH HHS/ -- T32 CA-009666/CA/NCI NIH HHS/ -- T32 CA009666/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2014 Oct 10;346(6206):256-9. doi: 10.1126/science.1256930.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genomic Medicine, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA. Department of Thoracic/Head and Neck Medical Oncology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA. ; Department of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA. ; Applied Cancer Science Institute, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA. ; Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton CB10 1SA, UK. ; Department of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA. ; Department of Genomic Medicine, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA. ; Department of Thoracic/Head and Neck Medical Oncology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA. ; Department of Pathology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA. ; Department of Epidemiology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA. ; Department of Biostatistics, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA. ; Department of Thoracic/Head and Neck Medical Oncology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA. Department of Cancer Biology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA. ; Department of Thoracic and Cardiovascular Surgery, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA. ; Department of Genomic Medicine, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA. Honorary Faculty, Wellcome Trust Sanger Institute, Hinxton, UK CB10 1SA. afutreal@mdanderson.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25301631" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/*genetics/pathology ; DNA Mutational Analysis ; Exome/genetics ; Genes, Neoplasm ; *Genetic Heterogeneity ; Humans ; Lung Neoplasms/*genetics/pathology ; Mutation ; Neoplasm Recurrence, Local/*genetics/pathology
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  • 20
    Publication Date: 2014-05-07
    Description: Parabiosis experiments indicate that impaired regeneration in aged mice is reversible by exposure to a young circulation, suggesting that young blood contains humoral "rejuvenating" factors that can restore regenerative function. Here, we demonstrate that the circulating protein growth differentiation factor 11 (GDF11) is a rejuvenating factor for skeletal muscle. Supplementation of systemic GDF11 levels, which normally decline with age, by heterochronic parabiosis or systemic delivery of recombinant protein, reversed functional impairments and restored genomic integrity in aged muscle stem cells (satellite cells). Increased GDF11 levels in aged mice also improved muscle structural and functional features and increased strength and endurance exercise capacity. These data indicate that GDF11 systemically regulates muscle aging and may be therapeutically useful for reversing age-related skeletal muscle and stem cell dysfunction.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4104429/" 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/PMC4104429/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sinha, Manisha -- Jang, Young C -- Oh, Juhyun -- Khong, Danika -- Wu, Elizabeth Y -- Manohar, Rohan -- Miller, Christine -- Regalado, Samuel G -- Loffredo, Francesco S -- Pancoast, James R -- Hirshman, Michael F -- Lebowitz, Jessica -- Shadrach, Jennifer L -- Cerletti, Massimiliano -- Kim, Mi-Jeong -- Serwold, Thomas -- Goodyear, Laurie J -- Rosner, Bernard -- Lee, Richard T -- Wagers, Amy J -- 1DP2 OD004345/OD/NIH HHS/ -- 1R01 AG033053/AG/NIA NIH HHS/ -- 1R01 AG040019/AG/NIA NIH HHS/ -- 5U01 HL100402/HL/NHLBI NIH HHS/ -- DP2 OD004345/OD/NIH HHS/ -- P30 AG038072/AG/NIA NIH HHS/ -- R01 AG032977/AG/NIA NIH HHS/ -- R01 AG033053/AG/NIA NIH HHS/ -- R01 AG040019/AG/NIA NIH HHS/ -- R01 AR042238/AR/NIAMS NIH HHS/ -- R01 AR42238/AR/NIAMS NIH HHS/ -- T32 DE007057/DE/NIDCR NIH HHS/ -- U01 HL100402/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 May 9;344(6184):649-52. doi: 10.1126/science.1251152. Epub 2014 May 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Harvard Stem Cell Institute and Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24797481" target="_blank"〉PubMed〈/a〉
    Keywords: Age Factors ; Aging/blood/drug effects/*physiology ; Animals ; Bone Morphogenetic Proteins/administration & dosage/blood/*physiology ; Growth Differentiation Factors/administration & dosage/blood/*physiology ; Male ; Mice ; Mice, Inbred C57BL ; Muscle, Skeletal/*blood supply/drug effects/*physiology ; Myoblasts, Skeletal/drug effects/*physiology ; Parabiosis ; *Regeneration ; *Rejuvenation
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  • 21
    Publication Date: 2014-02-08
    Description: Neuronal intracellular chloride concentration [Cl(-)](i) is an important determinant of gamma-aminobutyric acid type A (GABA(A)) receptor (GABA(A)R)-mediated inhibition and cytoplasmic volume regulation. Equilibrative cation-chloride cotransporters (CCCs) move Cl(-) across the membrane, but accumulating evidence suggests factors other than the bulk concentrations of transported ions determine [Cl(-)](i). Measurement of [Cl(-)](i) in murine brain slice preparations expressing the transgenic fluorophore Clomeleon demonstrated that cytoplasmic impermeant anions ([A](i)) and polyanionic extracellular matrix glycoproteins ([A](o)) constrain the local [Cl(-)]. CCC inhibition had modest effects on [Cl(-)](i) and neuronal volume, but substantial changes were produced by alterations of the balance between [A](i) and [A](o). Therefore, CCCs are important elements of Cl(-) homeostasis, but local impermeant anions determine the homeostatic set point for [Cl(-)], and hence, neuronal volume and the polarity of local GABA(A)R signaling.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4220679/" 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/PMC4220679/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Glykys, J -- Dzhala, V -- Egawa, K -- Balena, T -- Saponjian, Y -- Kuchibhotla, K V -- Bacskai, B J -- Kahle, K T -- Zeuthen, T -- Staley, K J -- NS 40109-06/NS/NINDS NIH HHS/ -- R01 EB000768/EB/NIBIB NIH HHS/ -- R01 NS040109/NS/NINDS NIH HHS/ -- R01 NS074772/NS/NINDS NIH HHS/ -- R25 NS065743/NS/NINDS NIH HHS/ -- S10 RR025645/RR/NCRR NIH HHS/ -- U41 RR019703/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2014 Feb 7;343(6171):670-5. doi: 10.1126/science.1245423.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24503855" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*metabolism ; Cell Membrane Permeability ; Cell Polarity ; Chloride Channels/*metabolism ; Chlorides/*metabolism ; Cytoplasm/metabolism ; Extracellular Matrix Proteins/metabolism ; Glycoproteins/metabolism ; Mice ; Mice, Transgenic ; Neurons/*metabolism ; Receptors, GABA-A/*metabolism ; Recombinant Fusion Proteins/genetics/metabolism ; Signal Transduction
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  • 22
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-03-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kean, Sam -- New York, N.Y. -- Science. 2014 Mar 28;343(6178):1457-9. doi: 10.1126/science.343.6178.1457.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24675950" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/*genetics ; Checkpoint Kinase 2/genetics ; Female ; Genes, BRCA1 ; Genes, BRCA2 ; *Genetic Predisposition to Disease ; Humans ; Mutation ; Nuclear Proteins/genetics ; *Oncogenes ; Tumor Suppressor Proteins/genetics
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  • 23
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-05-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, Elizabeth -- New York, N.Y. -- Science. 2014 May 23;344(6186):824-5. doi: 10.1126/science.344.6186.824.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24855252" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Botswana ; *Hierarchy, Social/history ; History, Ancient ; Hominidae/growth & development ; Humans ; *Life Style/ethnology/history ; Male ; *Social Behavior/history ; Socioeconomic Factors/history
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  • 24
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-03-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pringle, Heather -- New York, N.Y. -- Science. 2014 Feb 28;343(6174):961-3. doi: 10.1126/science.343.6174.961.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24578560" target="_blank"〉PubMed〈/a〉
    Keywords: *Animal Migration ; Animals ; Archaeology ; Arctic Regions ; Asian Continental Ancestry Group/*genetics ; *Cold Temperature ; DNA, Mitochondrial/genetics ; Deer/*genetics ; Genetic Variation ; *Human Migration ; Humans ; Ice Cover ; Indians, North American/*genetics ; Islands ; Mutation ; North America ; Rivers ; Siberia
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  • 25
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-02-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Promislow, Daniel E L -- Kaeberlein, Matt -- R01 AG031108/AG/NIA NIH HHS/ -- R01 AG033598/AG/NIA NIH HHS/ -- R01 GM102279/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2014 Jan 31;343(6170):491-2. doi: 10.1126/science.1250174.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Washington, Seattle, WA 98195 USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24482469" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/*physiology ; Drosophila melanogaster/*physiology ; Female ; Longevity/*physiology ; Male ; Pheromones/*physiology ; *Reward ; Sexual Behavior, Animal/*physiology ; Spermatozoa/*physiology ; *Taste Perception
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  • 26
    Publication Date: 2014-03-08
    Description: The excitatory neurotransmitter glutamate induces modulatory actions via the metabotropic glutamate receptors (mGlus), which are class C G protein-coupled receptors (GPCRs). We determined the structure of the human mGlu1 receptor seven-transmembrane (7TM) domain bound to a negative allosteric modulator, FITM, at a resolution of 2.8 angstroms. The modulator binding site partially overlaps with the orthosteric binding sites of class A GPCRs but is more restricted than most other GPCRs. We observed a parallel 7TM dimer mediated by cholesterols, which suggests that signaling initiated by glutamate's interaction with the extracellular domain might be mediated via 7TM interactions within the full-length receptor dimer. A combination of crystallography, structure-activity relationships, mutagenesis, and full-length dimer modeling provides insights about the allosteric modulation and activation mechanism of class C GPCRs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3991565/" 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/PMC3991565/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, Huixian -- Wang, Chong -- Gregory, Karen J -- Han, Gye Won -- Cho, Hyekyung P -- Xia, Yan -- Niswender, Colleen M -- Katritch, Vsevolod -- Meiler, Jens -- Cherezov, Vadim -- Conn, P Jeffrey -- Stevens, Raymond C -- P50 GM073197/GM/NIGMS NIH HHS/ -- R01 DK097376/DK/NIDDK NIH HHS/ -- R01 GM080403/GM/NIGMS NIH HHS/ -- R01 GM099842/GM/NIGMS NIH HHS/ -- R01 MH062646/MH/NIMH NIH HHS/ -- R01 MH090192/MH/NIMH NIH HHS/ -- R01 NS031373/NS/NINDS NIH HHS/ -- R21 NS078262/NS/NINDS NIH HHS/ -- R37 NS031373/NS/NINDS NIH HHS/ -- U54 GM094618/GM/NIGMS NIH HHS/ -- Y1-CO-1020/CO/NCI NIH HHS/ -- Y1-GM-1104/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2014 Apr 4;344(6179):58-64. doi: 10.1126/science.1249489. Epub 2014 Mar 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Integrative Structural and Computational Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24603153" target="_blank"〉PubMed〈/a〉
    Keywords: Allosteric Regulation ; Allosteric Site ; Amino Acid Sequence ; Benzamides/*chemistry/*metabolism ; Binding Sites ; Cholesterol ; Crystallography, X-Ray ; Humans ; Hydrophobic and Hydrophilic Interactions ; Ligands ; Models, Molecular ; Molecular Sequence Data ; Mutation ; Protein Conformation ; Protein Multimerization ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Receptors, Metabotropic Glutamate/*chemistry/*metabolism ; Structure-Activity Relationship ; Thiazoles/*chemistry/*metabolism
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  • 27
    Publication Date: 2014-01-25
    Description: Comparative genomic analyses have revealed that genes may arise from ancestrally nongenic sequence. However, the origin and spread of these de novo genes within populations remain obscure. We identified 142 segregating and 106 fixed testis-expressed de novo genes in a population sample of Drosophila melanogaster. These genes appear to derive primarily from ancestral intergenic, unexpressed open reading frames, with natural selection playing a significant role in their spread. These results reveal a heretofore unappreciated dynamism of gene content.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4391638/" 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/PMC4391638/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhao, Li -- Saelao, Perot -- Jones, Corbin D -- Begun, David J -- GM084056/GM/NIGMS NIH HHS/ -- R01 GM084056/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2014 Feb 14;343(6172):769-72. doi: 10.1126/science.1248286. Epub 2014 Jan 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Evolution and Ecology, University of California, Davis, CA 95616, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24457212" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Drosophila melanogaster/*genetics ; *Evolution, Molecular ; Female ; Gene Expression ; Gene Expression Regulation ; *Genes, Insect ; Genetic Association Studies ; Male ; Open Reading Frames ; Selection, Genetic ; Testis/metabolism
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  • 28
    Publication Date: 2014-04-05
    Description: Most land animals normally walk forward but switch to backward walking upon sensing an obstacle or danger in the path ahead. A change in walking direction is likely to be triggered by descending "command" neurons from the brain that act upon local motor circuits to alter the timing of leg muscle activation. Here we identify descending neurons for backward walking in Drosophila--the MDN neurons. MDN activity is required for flies to walk backward when they encounter an impassable barrier and is sufficient to trigger backward walking under conditions in which flies would otherwise walk forward. We also identify ascending neurons, MAN, that promote persistent backward walking, possibly by inhibiting forward walking. These findings provide an initial glimpse into the circuits and logic that control walking direction in Drosophila.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bidaye, Salil S -- Machacek, Christian -- Wu, Yang -- Dickson, Barry J -- New York, N.Y. -- Science. 2014 Apr 4;344(6179):97-101. doi: 10.1126/science.1249964.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Research Institute of Molecular Pathology (IMP), Dr. Bohrgasse 7, A-1030 Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24700860" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/cytology ; Drosophila/*physiology ; Extremities/physiology ; Female ; Gait ; Ganglia, Invertebrate/cytology ; Male ; Neurons/*physiology ; Walking/physiology
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  • 29
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-03-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bhattacharjee, Yudhijit -- New York, N.Y. -- Science. 2014 Mar 21;343(6177):1306-9. doi: 10.1126/science.343.6177.1306.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24653017" target="_blank"〉PubMed〈/a〉
    Keywords: Biological Evolution ; DNA, Intergenic/genetics ; Databases, Nucleic Acid ; *Genome, Human ; *Genomics ; History, 20th Century ; History, 21st Century ; Humans ; Molecular Sequence Annotation ; Mutation ; National Human Genome Research Institute (U.S.) ; Transcription Factors/metabolism ; Transcription, Genetic ; United States
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  • 30
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-01-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, Elizabeth -- New York, N.Y. -- Science. 2014 Jan 17;343(6168):239. doi: 10.1126/science.343.6168.239.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24436399" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ants/*microbiology/physiology ; Brain/metabolism/microbiology ; Fat Body/virology ; Female ; Gryllidae/physiology/*virology ; Guanidines/analysis/metabolism ; *Host-Pathogen Interactions ; Hypocreales/*physiology ; Insect Viruses/*physiology ; Lizards/virology ; Male ; Rats ; Sexual Behavior, Animal/*physiology ; Sphingosine/analysis/metabolism ; Virus Replication
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  • 31
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-04-26
    Description: How we attend to objects and their features that cannot be separated by location is not understood. We presented two temporally and spatially overlapping streams of objects, faces versus houses, and used magnetoencephalography and functional magnetic resonance imaging to separate neuronal responses to attended and unattended objects. Attention to faces versus houses enhanced the sensory responses in the fusiform face area (FFA) and parahippocampal place area (PPA), respectively. The increases in sensory responses were accompanied by induced gamma synchrony between the inferior frontal junction, IFJ, and either FFA or PPA, depending on which object was attended. The IFJ appeared to be the driver of the synchrony, as gamma phases were advanced by 20 ms in IFJ compared to FFA or PPA. Thus, the IFJ may direct the flow of visual processing during object-based attention, at least in part through coupled oscillations with specialized areas such as FFA and PPA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baldauf, Daniel -- Desimone, Robert -- P30EY2621/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 2014 Apr 25;344(6182):424-7. doi: 10.1126/science.1247003. Epub 2014 Apr 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉McGovern Institute for Brain Research, Massachusetts Institute of Technology, Cambridge, 02139 MA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24763592" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; *Attention ; Brain/*physiology ; Brain Mapping ; Diffusion Tensor Imaging ; Female ; Frontal Lobe/*physiology ; Functional Laterality ; Humans ; Magnetic Resonance Imaging ; Magnetoencephalography ; Male ; Temporal Lobe/*physiology ; Visual Cortex/physiology ; Visual Perception ; Young Adult
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  • 32
    Publication Date: 2014-07-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, Jon -- New York, N.Y. -- Science. 2014 Jul 11;345(6193):152-5. doi: 10.1126/science.345.6193.152. Epub 2014 Jul 10.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25013057" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/complications/*drug therapy/*epidemiology ; Anti-Retroviral Agents/*therapeutic use ; Australia/epidemiology ; Biomedical Research/trends ; Health Services Accessibility/*organization & administration ; Hospitals, Public ; Humans ; Male ; Middle Aged ; Pneumonia, Pneumocystis/etiology
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  • 33
    Publication Date: 2014-04-05
    Description: Development of vertebrate embryos involves tightly regulated molecular and cellular processes that progressively instruct proliferating embryonic cells about their identity and behavior. Whereas numerous gene activities have been found to be essential during early embryogenesis, little is known about the minimal conditions and factors that would be sufficient to instruct pluripotent cells to organize the embryo. Here, we show that opposing gradients of bone morphogenetic protein (BMP) and Nodal, two transforming growth factor family members that act as morphogens, are sufficient to induce molecular and cellular mechanisms required to organize, in vivo or in vitro, uncommitted cells of the zebrafish blastula animal pole into a well-developed embryo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xu, Peng-Fei -- Houssin, Nathalie -- Ferri-Lagneau, Karine F -- Thisse, Bernard -- Thisse, Christine -- New York, N.Y. -- Science. 2014 Apr 4;344(6179):87-9. doi: 10.1126/science.1248252.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, University of Virginia, Charlottesville, VA 22908, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24700857" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastula/*physiology ; Body Patterning ; Bone Morphogenetic Proteins/genetics/*physiology ; Embryo, Nonmammalian/*physiology ; *Embryonic Development ; Gastrula/physiology ; Gastrulation ; Gene Expression Regulation, Developmental ; Morphogenesis ; Nodal Protein/genetics/*physiology ; RNA, Messenger/genetics ; Signal Transduction ; Zebrafish/*embryology/genetics ; Zebrafish Proteins/genetics/*physiology
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  • 34
    Publication Date: 2014-05-24
    Description: Decisions take time if information gradually accumulates to a response threshold, but the neural mechanisms of integration and thresholding are unknown. We characterized a decision process in Drosophila that bears the behavioral signature of evidence accumulation. As stimulus contrast in trained odor discriminations decreased, reaction times increased and perceptual accuracy declined, in quantitative agreement with a drift-diffusion model. FoxP mutants took longer than wild-type flies to form decisions of similar or reduced accuracy, especially in difficult, low-contrast tasks. RNA interference with FoxP expression in alphabeta core Kenyon cells, or the overexpression of a potassium conductance in these neurons, recapitulated the FoxP mutant phenotype. A mushroom body subdomain whose development or function require the transcription factor FoxP thus supports the progression of a decision toward commitment.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4206523/" 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/PMC4206523/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉DasGupta, Shamik -- Ferreira, Clara Howcroft -- Miesenbock, Gero -- 090309/Wellcome Trust/United Kingdom -- G0700888/Medical Research Council/United Kingdom -- G0701225/Medical Research Council/United Kingdom -- R01 DA030601/DA/NIDA NIH HHS/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2014 May 23;344(6186):901-4. doi: 10.1126/science.1252114.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Neural Circuits and Behaviour, University of Oxford, Tinsley Building, Mansfield Road, Oxford, OX1 3SR, UK. ; Centre for Neural Circuits and Behaviour, University of Oxford, Tinsley Building, Mansfield Road, Oxford, OX1 3SR, UK. gero.miesenboeck@cncb.ox.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24855268" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Behavior, Animal ; Cell Line ; *Decision Making ; Drosophila Proteins/genetics/*physiology ; Drosophila melanogaster/genetics/*physiology ; Forkhead Transcription Factors/genetics/*physiology ; Mushroom Bodies/growth & development/metabolism ; Mutation ; Neurons/physiology ; Odors ; *Psychomotor Performance ; RNA Interference ; Reaction Time/genetics/*physiology ; Smell
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  • 35
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-02-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Blair, H T -- New York, N.Y. -- Science. 2014 Feb 21;343(6173):846-7. doi: 10.1126/science.1251252.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Psychology Department and Brain Research Institute, University of California, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24558150" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Association ; CA1 Region, Hippocampal/*physiology ; Entorhinal Cortex/*cytology/*physiology ; Female ; Male ; *Memory, Episodic ; *Nerve Net ; Neurons/*physiology ; Pyramidal Cells/*physiology/*ultrastructure ; *Theta Rhythm
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  • 36
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-04-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McConnell, William J -- Kull, Christian A -- New York, N.Y. -- Science. 2014 Apr 25;344(6182):358. doi: 10.1126/science.344.6182.358-a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Systems Integration and Sustainability, Michigan State University, East Lansing, MI 48823, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24763569" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Endangered Species ; *Extinction, Biological ; *Lemur ; Male
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  • 37
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-03-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Balter, Michael -- New York, N.Y. -- Science. 2014 Mar 14;343(6176):1190-3. doi: 10.1126/science.343.6176.1190.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24626910" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Affective Symptoms/therapy ; Antipsychotic Agents/adverse effects/therapeutic use ; Cognitive Therapy/*methods ; Delusions/therapy ; Drug Discovery ; Genes ; Hallucinations/therapy ; Humans ; Male ; Middle Aged ; Placebo Effect ; Psychotherapy, Psychodynamic/*methods ; Randomized Controlled Trials as Topic ; Schizophrenia/drug therapy/genetics/*therapy
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  • 38
    Publication Date: 2014-12-17
    Description: Sex-specific chromosomes, like the W of most female birds and the Y of male mammals, usually have lost most genes owing to a lack of recombination. We analyze newly available genomes of 17 bird species representing the avian phylogenetic range, and find that more than half of them do not have as fully degenerated W chromosomes as that of chicken. We show that avian sex chromosomes harbor tremendous diversity among species in their composition of pseudoautosomal regions and degree of Z/W differentiation. Punctuated events of shared or lineage-specific recombination suppression have produced a gradient of "evolutionary strata" along the Z chromosome, which initiates from the putative avian sex-determining gene DMRT1 and ends at the pseudoautosomal region. W-linked genes are subject to ongoing functional decay after recombination was suppressed, and the tempo of degeneration slows down in older strata. Overall, we unveil a complex history of avian sex chromosome evolution.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, Qi -- Zhang, Jilin -- Bachtrog, Doris -- An, Na -- Huang, Quanfei -- Jarvis, Erich D -- Gilbert, M Thomas P -- Zhang, Guojie -- GM076007/GM/NIGMS NIH HHS/ -- GM093182/GM/NIGMS NIH HHS/ -- R01 GM076007/GM/NIGMS NIH HHS/ -- R01 GM093182/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Dec 12;346(6215):1246338. doi: 10.1126/science.1246338. Epub 2014 Dec 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Integrative Biology, University of California, Berkeley, CA94720, USA. zhouqi@berkeley.edu zhanggj@genomics.org.cn. ; China National Genebank, BGI-Shenzhen, Shenzhen, 518083. China. ; Department of Integrative Biology, University of California, Berkeley, CA94720, USA. ; Department of Neurobiology, Howard Hughes Medical Institute, Duke University Medical Center, Durham, NC 27710, USA. ; Centre for GeoGenetics, Natural History Museum of Denmark, University of Copenhagen, Oster Voldgade 5-7, 1350 Copenhagen, Denmark. Trace and Environmental DNA laboratory, Department of Environment and Agriculture, Curtin University, Perth, Western Australia 6102, Australia. ; China National Genebank, BGI-Shenzhen, Shenzhen, 518083. China. Centre for Social Evolution, Department of Biology, Universitetsparken 15, University of Copenhagen, DK-2100 Copenhagen, Denmark. zhouqi@berkeley.edu zhanggj@genomics.org.cn.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25504727" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Avian Proteins/genetics ; *Biological Evolution ; Birds/classification/*genetics ; Chickens/genetics ; Chromosome Inversion ; Chromosome Mapping ; *Evolution, Molecular ; Female ; Male ; Phylogeny ; Recombination, Genetic ; Sex Chromosomes/*genetics ; Species Specificity ; Struthioniformes/genetics ; Synteny ; Transcription Factors/genetics
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  • 39
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-02-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Balter, Michael -- New York, N.Y. -- Science. 2014 Feb 14;343(6172):716-7. doi: 10.1126/science.343.6172.716.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24531945" target="_blank"〉PubMed〈/a〉
    Keywords: Archaeology ; Emigrants and Immigrants/history ; Genome, Human/*genetics ; History, Ancient ; Humans ; Indians, North American/*genetics/history ; Infant ; Male ; Montana ; Sequence Analysis, DNA ; Skull
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  • 40
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-08-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Susiarjo, Martha -- Bartolomei, Marisa S -- P30 ES013508/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 2014 Aug 15;345(6198):733-4. doi: 10.1126/science.1258654.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. ; Department of Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. bartolom@mail.med.upenn.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25124413" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *DNA Methylation ; Female ; Fetal Nutrition Disorders/*metabolism ; Male ; Pregnancy ; *Prenatal Exposure Delayed Effects ; Spermatozoa/*metabolism
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  • 41
    Publication Date: 2014-06-07
    Description: How sleep helps learning and memory remains unknown. We report in mouse motor cortex that sleep after motor learning promotes the formation of postsynaptic dendritic spines on a subset of branches of individual layer V pyramidal neurons. New spines are formed on different sets of dendritic branches in response to different learning tasks and are protected from being eliminated when multiple tasks are learned. Neurons activated during learning of a motor task are reactivated during subsequent non-rapid eye movement sleep, and disrupting this neuronal reactivation prevents branch-specific spine formation. These findings indicate that sleep has a key role in promoting learning-dependent synapse formation and maintenance on selected dendritic branches, which contribute to memory storage.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4447313/" 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/PMC4447313/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, Guang -- Lai, Cora Sau Wan -- Cichon, Joseph -- Ma, Lei -- Li, Wei -- Gan, Wen-Biao -- P01 NS074972/NS/NINDS NIH HHS/ -- R01 NS047325/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2014 Jun 6;344(6188):1173-8. doi: 10.1126/science.1249098.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Skirball Institute, Department of Neuroscience and Physiology, New York University School of Medicine, New York, NY 10016, USA. Department of Anesthesiology, New York University School of Medicine, New York, NY 10016, USA. ; Skirball Institute, Department of Neuroscience and Physiology, New York University School of Medicine, New York, NY 10016, USA. ; Skirball Institute, Department of Neuroscience and Physiology, New York University School of Medicine, New York, NY 10016, USA. Drug Discovery Center, Key Laboratory of Chemical Genomics, Peking University Shenzhen Graduate School, Shenzhen, 518055, China. ; Drug Discovery Center, Key Laboratory of Chemical Genomics, Peking University Shenzhen Graduate School, Shenzhen, 518055, China. ; Skirball Institute, Department of Neuroscience and Physiology, New York University School of Medicine, New York, NY 10016, USA. gan@saturn.med.nyu.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24904169" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dendritic Spines/*physiology ; Female ; Learning/*physiology ; Male ; Mice ; Mice, Mutant Strains ; Motor Cortex/*physiology ; Sleep, REM/*physiology
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  • 42
    Publication Date: 2014-10-18
    Description: Myelin-forming oligodendrocytes (OLs) are formed continuously in the healthy adult brain. In this work, we study the function of these late-forming cells and the myelin they produce. Learning a new motor skill (such as juggling) alters the structure of the brain's white matter, which contains many OLs, suggesting that late-born OLs might contribute to motor learning. Consistent with this idea, we show that production of newly formed OLs is briefly accelerated in mice that learn a new skill (running on a "complex wheel" with irregularly spaced rungs). By genetically manipulating the transcription factor myelin regulatory factor in OL precursors, we blocked production of new OLs during adulthood without affecting preexisting OLs or myelin. This prevented the mice from mastering the complex wheel. Thus, generation of new OLs and myelin is important for learning motor skills.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McKenzie, Ian A -- Ohayon, David -- Li, Huiliang -- de Faria, Joana Paes -- Emery, Ben -- Tohyama, Koujiro -- Richardson, William D -- 100269/Wellcome Trust/United Kingdom -- G0800575/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2014 Oct 17;346(6207):318-22. doi: 10.1126/science.1254960.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Wolfson Institute for Biomedical Research, University College London, Gower Street, London WC1E 6BT, UK. ; Department of Anatomy and Neuroscience and the Florey Institute for Neuroscience and Mental Health, University of Melbourne, Melbourne, Victoria 3010, Australia. ; The Center for Electron Microscopy and Bio-Imaging Research, Iwate Medical University, 19-1 Uchimuru, Morioka, Iwate 020-8505, Japan. ; The Wolfson Institute for Biomedical Research, University College London, Gower Street, London WC1E 6BT, UK. w.richardson@ucl.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25324381" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*cytology/metabolism ; *Cell Proliferation ; Gene Deletion ; Humans ; *Learning ; Male ; Mental Recall ; Mice ; Mice, Transgenic ; Motor Skills/*physiology ; Myelin Sheath/genetics/*metabolism ; Oligodendroglia/cytology/metabolism/*physiology ; Synaptic Transmission ; Transcription Factors/genetics/metabolism
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  • 43
    Publication Date: 2014-05-17
    Description: Environmental exposures affect gamete function and fertility, but the mechanisms are poorly understood. Here, we show that pheromones sensed by ciliated neurons in the Caenorhabditis elegans nose alter the lipid microenvironment within the oviduct, thereby affecting sperm motility. In favorable environments, pheromone-responsive sensory neurons secrete a transforming growth factor-beta ligand called DAF-7, which acts as a neuroendocrine factor that stimulates prostaglandin-endoperoxide synthase [cyclooxygenase (Cox)]-independent prostaglandin synthesis in the ovary. Oocytes secrete F-class prostaglandins that guide sperm toward them. These prostaglandins are also synthesized in Cox knockout mice, raising the possibility that similar mechanisms exist in other animals. Our data indicate that environmental cues perceived by the female nervous system affect sperm function.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4094289/" 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/PMC4094289/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McKnight, Katherine -- Hoang, Hieu D -- Prasain, Jeevan K -- Brown, Naoko -- Vibbert, Jack -- Hollister, Kyle A -- Moore, Ray -- Ragains, Justin R -- Reese, Jeff -- Miller, Michael A -- GM085105/GM/NIGMS NIH HHS/ -- HL096967/HL/NHLBI NIH HHS/ -- HL109199/HL/NHLBI NIH HHS/ -- HL110950/HL/NHLBI NIH HHS/ -- HL114439/HL/NHLBI NIH HHS/ -- P30 AR050948/AR/NIAMS NIH HHS/ -- P30 DK079337/DK/NIDDK NIH HHS/ -- P40 OD010440/OD/NIH HHS/ -- R01 GM085105/GM/NIGMS NIH HHS/ -- R01 HL096967/HL/NHLBI NIH HHS/ -- R01 HL109199/HL/NHLBI NIH HHS/ -- S10 RR19261/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2014 May 16;344(6185):754-7. doi: 10.1126/science.1250598.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, University of Alabama at Birmingham, Birmingham, AL 35294, USA. ; Department of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL 35294, USA. ; Department of Pharmacology and Toxicology, University of Alabama at Birmingham, Birmingham, AL 35294, USA. ; Department of Pediatrics, Vanderbilt University, Nashville, TN 37232, USA. ; Department of Chemistry, Louisiana State University, Baton Rouge, LA 70803, USA. ; Department of Pediatrics, Vanderbilt University, Nashville, TN 37232, USA. Department of Cell and Developmental Biology, Vanderbilt University, Nashville, TN 37232, USA. ; Department of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL 35294, USA. mamiller@uab.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24833393" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/genetics/metabolism/*physiology ; Caenorhabditis elegans Proteins/genetics/*metabolism ; Environmental Exposure ; Female ; *Fertilization ; Male ; Neurons, Afferent/*physiology ; Neurosecretory Systems/physiology ; Oocytes/metabolism/physiology ; Ovum/metabolism/physiology ; Perception ; Pheromones/*physiology ; Prostaglandin-Endoperoxide Synthases/metabolism ; Prostaglandins/biosynthesis ; *Sperm Motility ; Spermatozoa/*physiology ; Transforming Growth Factor beta/genetics/*metabolism
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  • 44
    Publication Date: 2014-12-06
    Description: Immune and inflammatory responses require leukocytes to migrate within and through the vasculature, a process that is facilitated by their capacity to switch to a polarized morphology with an asymmetric distribution of receptors. We report that neutrophil polarization within activated venules served to organize a protruding domain that engaged activated platelets present in the bloodstream. The selectin ligand PSGL-1 transduced signals emanating from these interactions, resulting in the redistribution of receptors that drive neutrophil migration. Consequently, neutrophils unable to polarize or to transduce signals through PSGL-1 displayed aberrant crawling, and blockade of this domain protected mice against thromboinflammatory injury. These results reveal that recruited neutrophils scan for activated platelets, and they suggest that the neutrophils' bipolarity allows the integration of signals present at both the endothelium and the circulation before inflammation proceeds.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4280847/" 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/PMC4280847/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sreeramkumar, Vinatha -- Adrover, Jose M -- Ballesteros, Ivan -- Cuartero, Maria Isabel -- Rossaint, Jan -- Bilbao, Izaskun -- Nacher, Maria -- Pitaval, Christophe -- Radovanovic, Irena -- Fukui, Yoshinori -- McEver, Rodger P -- Filippi, Marie-Dominique -- Lizasoain, Ignacio -- Ruiz-Cabello, Jesus -- Zarbock, Alexander -- Moro, Maria A -- Hidalgo, Andres -- HL03463/HL/NHLBI NIH HHS/ -- HL085607/HL/NHLBI NIH HHS/ -- HL090676/HL/NHLBI NIH HHS/ -- P01 HL085607/HL/NHLBI NIH HHS/ -- R01 HL034363/HL/NHLBI NIH HHS/ -- R01 HL090676/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2014 Dec 5;346(6214):1234-8. doi: 10.1126/science.1256478. Epub 2014 Dec 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Atherothrombosis, Imaging and Epidemiology, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain. ; Unidad de Investigacion Neurovascular, Department of Pharmacology, Faculty of Medicine, Universidad Complutense and Instituto de Investigacion Hospital 12 de Octubre (i+12), Madrid, Spain. ; Department of Anesthesiology and Critical Care Medicine, University of Munster and Max Planck Institute Munster, Munster, Germany. ; Department of Atherothrombosis, Imaging and Epidemiology, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain. Ciber de Enfermedades Respiratorias (CIBERES), Madrid, Spain. ; Department of Atherothrombosis, Imaging and Epidemiology, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain. Faculty of Science, Medicine and Health, University of Wollongong, New South Wales, Australia. ; Division of Immunogenetics, Department of Immunobiology and Neuroscience, Kyushu University, Japan. ; Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA. ; Division of Experimental Hematology and Cancer Biology, Cincinnati Children's Research Foundation, University of Cincinnati College of Medicine, Cincinnati, OH, USA. ; Department of Atherothrombosis, Imaging and Epidemiology, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain. Institute for Cardiovascular Prevention, Ludwig-Maximilians-University, Munich, Germany. ahidalgo@cnic.es.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25477463" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Circulation ; Blood Platelets/*immunology ; Cell Movement ; Cell Polarity ; Endothelium, Vascular/immunology ; Inflammation/blood/*immunology ; Male ; Membrane Glycoproteins ; Mice ; Mice, Inbred C57BL ; Neutrophils/*immunology ; *Platelet Activation ; Signal Transduction ; Thrombosis/*immunology ; Venules/immunology
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  • 45
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-06-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Szyszka, Paul -- New York, N.Y. -- Science. 2014 Jun 27;344(6191):1454. doi: 10.1126/science.1255748.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, University of Konstanz, 78457 Konstanz, Germany. paul.szyszka@uni-konstanz.de.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24970067" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Datura/*physiology ; Flowers/*physiology ; Male ; Manduca/*physiology ; Neurons/*physiology ; *Odors ; Olfactory Receptor Neurons/*physiology
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  • 46
    Publication Date: 2014-10-18
    Description: Nitrogen (N) is a critical nutrient for plants but is often distributed unevenly in the soil. Plants therefore have evolved a systemic mechanism by which N starvation on one side of the root system leads to a compensatory and increased nitrate uptake on the other side. Here, we study the molecular systems that support perception of N and the long-distance signaling needed to alter root development. Rootlets starved of N secrete small peptides that are translocated to the shoot and received by two leucine-rich repeat receptor kinases (LRR-RKs). Arabidopsis plants deficient in this pathway show growth retardation accompanied with N-deficiency symptoms. Thus, signaling from the root to the shoot helps the plant adapt to fluctuations in local N availability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tabata, Ryo -- Sumida, Kumiko -- Yoshii, Tomoaki -- Ohyama, Kentaro -- Shinohara, Hidefumi -- Matsubayashi, Yoshikatsu -- New York, N.Y. -- Science. 2014 Oct 17;346(6207):343-6. doi: 10.1126/science.1257800.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biological Science, Graduate School of Science, Nagoya University, Chikusa, Nagoya 464-8602, Japan. ; Department of Applied Molecular Biosciences, Graduate School of Bio-Agricultural Sciences, Nagoya University, Chikusa, Nagoya 464-8601, Japan. ; Division of Biological Science, Graduate School of Science, Nagoya University, Chikusa, Nagoya 464-8602, Japan. matsu@bio.nagoya-u.ac.jp.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25324386" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Arabidopsis/genetics/*growth & development/metabolism ; Arabidopsis Proteins/genetics/*metabolism ; Molecular Sequence Data ; Nitrogen/*metabolism ; Peptides/*metabolism ; Plant Roots/genetics/*growth & development/metabolism ; Plant Shoots/genetics/*growth & development/metabolism ; Receptors, Peptide/genetics/*metabolism ; Signal Transduction
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  • 47
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-01-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Vrieze, Jop -- New York, N.Y. -- Science. 2014 Jan 17;343(6168):241-3. doi: 10.1126/science.343.6168.241.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24436401" target="_blank"〉PubMed〈/a〉
    Keywords: Anthropology ; Diabetes Mellitus, Type 1/immunology/microbiology ; Feces/microbiology ; Female ; Gastrointestinal Tract/*microbiology ; Germ-Free Life ; Health ; Humans ; *Life Style ; Male ; Meat/microbiology ; *Microbiota ; Tanzania
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  • 48
    Publication Date: 2014-07-26
    Description: Proteins that cap the ends of the actin filament are essential regulators of cytoskeleton dynamics. Whereas several proteins cap the rapidly growing barbed end, tropomodulin (Tmod) is the only protein known to cap the slowly growing pointed end. The lack of structural information severely limits our understanding of Tmod's capping mechanism. We describe crystal structures of actin complexes with the unstructured amino-terminal and the leucine-rich repeat carboxy-terminal domains of Tmod. The structures and biochemical analysis of structure-inspired mutants showed that one Tmod molecule interacts with three actin subunits at the pointed end, while also contacting two tropomyosin molecules on each side of the filament. We found that Tmod achieves high-affinity binding through several discrete low-affinity interactions, which suggests a mechanism for controlled subunit exchange at the pointed end.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4367809/" 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/PMC4367809/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rao, Jampani Nageswara -- Madasu, Yadaiah -- Dominguez, Roberto -- GM-0080/GM/NIGMS NIH HHS/ -- R01 GM073791/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2014 Jul 25;345(6195):463-7. doi: 10.1126/science.1256159.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. ; Department of Physiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. droberto@mail.med.upenn.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25061212" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/*chemistry ; Actins/*chemistry ; Amino Acid Sequence ; Animals ; Crystallography, X-Ray ; Humans ; Molecular Sequence Data ; Mutation ; Protein Binding ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Rabbits ; Tropomodulin/*chemistry/genetics
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  • 49
    Publication Date: 2014-05-09
    Description: Cross-cultural psychologists have mostly contrasted East Asia with the West. However, this study shows that there are major psychological differences within China. We propose that a history of farming rice makes cultures more interdependent, whereas farming wheat makes cultures more independent, and these agricultural legacies continue to affect people in the modern world. We tested 1162 Han Chinese participants in six sites and found that rice-growing southern China is more interdependent and holistic-thinking than the wheat-growing north. To control for confounds like climate, we tested people from neighboring counties along the rice-wheat border and found differences that were just as large. We also find that modernization and pathogen prevalence theories do not fit the data.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Talhelm, T -- Zhang, X -- Oishi, S -- Shimin, C -- Duan, D -- Lan, X -- Kitayama, S -- New York, N.Y. -- Science. 2014 May 9;344(6184):603-8. doi: 10.1126/science.1246850.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, University of Virginia, Charlottesville, VA 22904, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24812395" target="_blank"〉PubMed〈/a〉
    Keywords: *Agriculture ; Asian Continental Ancestry Group/*psychology ; China ; Female ; Humans ; *Individuation ; Male ; *Oryza ; *Triticum
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  • 50
    Publication Date: 2014-09-06
    Description: Pathogens traverse multiple barriers during infection, including cell membranes. We found that during this transition, pathogens carried covalently attached complement C3 into the cell, triggering immediate signaling and effector responses. Sensing of C3 in the cytosol activated mitochondrial antiviral signaling (MAVS)-dependent signaling cascades and induced proinflammatory cytokine secretion. C3 also flagged viruses for rapid proteasomal degradation, preventing their replication. This system could detect both viral and bacterial pathogens but was antagonized by enteroviruses, such as rhinovirus and poliovirus, which cleave C3 using their 3C protease. The antiviral rupintrivir inhibited 3C protease and prevented C3 cleavage, rendering enteroviruses susceptible to intracellular complement sensing. Thus, complement C3 allows cells to detect and disable pathogens that have invaded the cytosol.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4172439/" 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/PMC4172439/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tam, Jerry C H -- Bidgood, Susanna R -- McEwan, William A -- James, Leo C -- 281627/European Research Council/International -- MC_U105181010/Medical Research Council/United Kingdom -- U105181010/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2014 Sep 5;345(6201):1256070. doi: 10.1126/science.1256070. Epub 2014 Sep 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council Laboratory of Molecular Biology, Division of Protein and Nucleic Acid Chemistry, Francis Crick Avenue, Cambridge Biomedical Campus, Cambridge CB2 0QH, UK. ; Medical Research Council Laboratory of Molecular Biology, Division of Protein and Nucleic Acid Chemistry, Francis Crick Avenue, Cambridge Biomedical Campus, Cambridge CB2 0QH, UK. lcj@mrc-lmb.cam.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25190799" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/*immunology ; Adenovirus Infections, Human/*immunology ; Animals ; Antibodies, Viral/immunology ; Complement C3/*immunology ; Cytokines/biosynthesis/genetics ; Dogs ; HEK293 Cells ; Host-Pathogen Interactions/*immunology ; Humans ; *Immunity, Innate ; Interferon Regulatory Factors/metabolism ; NF-kappa B/metabolism ; Proteasome Endopeptidase Complex/metabolism ; Ribonucleoproteins/genetics/metabolism ; Signal Transduction ; Transcription Factor AP-1/metabolism
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  • 51
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-05-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kupferschmidt, Kai -- New York, N.Y. -- Science. 2014 May 2;344(6183):457-8. doi: 10.1126/science.344.6183.457.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24786052" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Camels/virology ; Communicable Diseases, Emerging/*epidemiology/*transmission/virology ; Coronavirus/genetics/*isolation & purification ; *Disease Outbreaks ; Food Contamination ; Genome, Viral ; Humans ; Meat/virology ; Milk/virology ; Mutation ; Risk Assessment ; Saudi Arabia/epidemiology ; Severe Acute Respiratory Syndrome/*epidemiology/*transmission/virology ; Species Specificity
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  • 52
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-08-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McNutt, Marcia -- New York, N.Y. -- Science. 2014 Aug 15;345(6198):739. doi: 10.1126/science.345.6198.739-b. Epub 2014 Aug 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Editor-in-Chief.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25124417" target="_blank"〉PubMed〈/a〉
    Keywords: Female ; *HIV Infections ; Humans ; Male ; *Periodicals as Topic ; *Sex Workers ; *Transgender Persons
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  • 53
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-12-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bar-Peled, Liron -- New York, N.Y. -- Science. 2014 Dec 5;346(6214):1191-2. doi: 10.1126/science.aaa1808.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Scripps Research Institute, La Jolla, CA 92122, USA. lironbp@scripps.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25477447" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acids/*metabolism ; Animals ; *Body Size ; *Cell Enlargement ; *Cell Proliferation ; GTP-Binding Protein Regulators/*metabolism ; Lysosomes/*metabolism ; Monomeric GTP-Binding Proteins/*metabolism ; Multiprotein Complexes/metabolism ; Protein Transport ; Signal Transduction ; TOR Serine-Threonine Kinases/metabolism
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  • 54
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-09-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉You, Jia -- New York, N.Y. -- Science. 2014 Sep 19;345(6203):1440-1. doi: 10.1126/science.345.6203.1440.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25237081" target="_blank"〉PubMed〈/a〉
    Keywords: *Communication ; Female ; Humans ; Male ; Research Personnel/*classification/*psychology ; *Science ; Sex Factors ; *Social Media
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  • 55
    Publication Date: 2014-05-24
    Description: Cushing's syndrome is caused by excess cortisol production from the adrenocortical gland. In corticotropin-independent Cushing's syndrome, the excess cortisol production is primarily attributed to an adrenocortical adenoma, in which the underlying molecular pathogenesis has been poorly understood. We report a hotspot mutation (L206R) in PRKACA, which encodes the catalytic subunit of cyclic adenosine monophosphate (cAMP)-dependent protein kinase (PKA), in more than 50% of cases with adrenocortical adenomas associated with corticotropin-independent Cushing's syndrome. The L206R PRKACA mutant abolished its binding to the regulatory subunit of PKA (PRKAR1A) that inhibits catalytic activity of PRKACA, leading to constitutive, cAMP-independent PKA activation. These results highlight the major role of cAMP-independent activation of cAMP/PKA signaling by somatic mutations in corticotropin-independent Cushing's syndrome, providing insights into the diagnosis and therapeutics of this syndrome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sato, Yusuke -- Maekawa, Shigekatsu -- Ishii, Ryohei -- Sanada, Masashi -- Morikawa, Teppei -- Shiraishi, Yuichi -- Yoshida, Kenichi -- Nagata, Yasunobu -- Sato-Otsubo, Aiko -- Yoshizato, Tetsuichi -- Suzuki, Hiromichi -- Shiozawa, Yusuke -- Kataoka, Keisuke -- Kon, Ayana -- Aoki, Kosuke -- Chiba, Kenichi -- Tanaka, Hiroko -- Kume, Haruki -- Miyano, Satoru -- Fukayama, Masashi -- Nureki, Osamu -- Homma, Yukio -- Ogawa, Seishi -- New York, N.Y. -- Science. 2014 May 23;344(6186):917-20. doi: 10.1126/science.1252328.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan. Department of Urology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. ; Department of Urology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. ; Department of Biophysics and Biochemistry, Graduate School of Science, The University of Tokyo, Tokyo, Japan. ; Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan. ; Department of Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. ; Laboratory of DNA Information Analysis, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan. ; Laboratory of Sequence Analysis, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan. ; Laboratory of DNA Information Analysis, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan. Laboratory of Sequence Analysis, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan. ; Department of Urology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. sogawa-tky@umin.ac.jp homma-uro@umin.ac.jp. ; Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan. sogawa-tky@umin.ac.jp homma-uro@umin.ac.jp.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24855271" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Cortex Neoplasms/*genetics ; Adrenocortical Adenoma/*genetics ; Adrenocorticotropic Hormone/metabolism ; Animals ; Catalytic Domain/genetics ; Cushing Syndrome/*genetics/metabolism ; Cyclic AMP-Dependent Protein Kinase Catalytic Subunits/*genetics/metabolism ; DNA Mutational Analysis ; GTP-Binding Protein alpha Subunits/genetics ; HEK293 Cells ; Humans ; Mice ; Mutation ; NIH 3T3 Cells ; PC12 Cells ; Rats
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  • 56
    Publication Date: 2014-01-18
    Description: Transcription factors (TFs) are key players in evolution. Changes affecting their function can yield novel life forms but may also have deleterious effects. Consequently, gene duplication events that release one gene copy from selective pressure are thought to be the common mechanism by which TFs acquire new activities. Here, we show that LEAFY, a major regulator of flower development and cell division in land plants, underwent changes to its DNA binding specificity, even though plant genomes generally contain a single copy of the LEAFY gene. We examined how these changes occurred at the structural level and identify an intermediate LEAFY form in hornworts that appears to adopt all different specificities. This promiscuous intermediate could have smoothed the evolutionary transitions, thereby allowing LEAFY to evolve new binding specificities while remaining a single-copy gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sayou, Camille -- Monniaux, Marie -- Nanao, Max H -- Moyroud, Edwige -- Brockington, Samuel F -- Thevenon, Emmanuel -- Chahtane, Hicham -- Warthmann, Norman -- Melkonian, Michael -- Zhang, Yong -- Wong, Gane Ka-Shu -- Weigel, Detlef -- Parcy, Francois -- Dumas, Renaud -- New York, N.Y. -- Science. 2014 Feb 7;343(6171):645-8. doi: 10.1126/science.1248229. Epub 2014 Jan 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CNRS, Laboratoire de Physiologie Cellulaire et Vegetale (LPCV), UMR 5168, 38054 Grenoble, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24436181" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Arabidopsis Proteins/chemistry/classification/genetics ; DNA, Plant/*chemistry ; DNA-Binding Proteins/*chemistry/classification/*genetics ; Electrophoretic Mobility Shift Assay ; *Evolution, Molecular ; Gene Dosage ; Molecular Sequence Data ; Mutation ; Phylogeny ; Plant Proteins/*chemistry/classification/*genetics ; Protein Binding/genetics ; Protein Structure, Tertiary ; Species Specificity ; Transcription Factors/chemistry/classification/genetics
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  • 57
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-08-16
    Description: Parental care, including feeding and protection of young, is essential for the survival as well as mental and physical well-being of the offspring. A large variety of parental behaviors has been described across species and sexes, raising fascinating questions about how animals identify the young and how brain circuits drive and modulate parental displays in males and females. Recent studies have begun to uncover a striking antagonistic interplay between brain systems underlying parental care and infant-directed aggression in both males and females, as well as a large range of intrinsic and environmentally driven neural modulation and plasticity. Improved understanding of the neural control of parental interactions in animals should provide novel insights into the complex issue of human parental care in both health and disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4230532/" 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/PMC4230532/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dulac, Catherine -- O'Connell, Lauren A -- Wu, Zheng -- R01 DC009019/DC/NIDCD NIH HHS/ -- R01 DC013087/DC/NIDCD NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Aug 15;345(6198):765-70. doi: 10.1126/science.1253291. Epub 2014 Aug 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Molecular and Cellular Biology, Center for Brain Science, Harvard University, Cambridge, MA 02138, USA. dulac@fas.harvard.edu. ; FAS Center for System Biology, Harvard University, Cambridge, MA 02138, USA. ; Howard Hughes Medical Institute, Department of Molecular and Cellular Biology, Center for Brain Science, Harvard University, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25124430" target="_blank"〉PubMed〈/a〉
    Keywords: Aggression ; Animals ; Biological Evolution ; Brain/*physiology ; Cues ; Female ; Humans ; Male ; Maternal Behavior/*physiology ; Models, Neurological ; Neural Pathways/physiology ; Neurons/physiology ; *Parenting ; Paternal Behavior/*physiology ; Sensation/*physiology
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  • 58
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-06-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morell, Virginia -- New York, N.Y. -- Science. 2014 Jun 20;344(6190):1334-7. doi: 10.1126/science.344.6190.1334.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24948718" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chiroptera/*physiology ; Female ; Humans ; Male ; Sexual Behavior, Animal/*physiology ; Speech/physiology/radiation effects ; *Vocalization, Animal
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  • 59
    Publication Date: 2014-08-30
    Description: Histone H3 lysine(27)-to-methionine (H3K27M) gain-of-function mutations occur in highly aggressive pediatric gliomas. We established a Drosophila animal model for the pathogenic histone H3K27M mutation and show that its overexpression resembles polycomb repressive complex 2 (PRC2) loss-of-function phenotypes, causing derepression of PRC2 target genes and developmental perturbations. Similarly, an H3K9M mutant depletes H3K9 methylation levels and suppresses position-effect variegation in various Drosophila tissues. The histone H3K9 demethylase KDM3B/JHDM2 associates with H3K9M-containing nucleosomes, and its misregulation in Drosophila results in changes of H3K9 methylation levels and heterochromatic silencing defects. We have established histone lysine-to-methionine mutants as robust in vivo tools for inhibiting methylation pathways that also function as biochemical reagents for capturing site-specific histone-modifying enzymes, thus providing molecular insight into chromatin signaling pathways.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4508193/" 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/PMC4508193/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Herz, Hans-Martin -- Morgan, Marc -- Gao, Xin -- Jackson, Jessica -- Rickels, Ryan -- Swanson, Selene K -- Florens, Laurence -- Washburn, Michael P -- Eissenberg, Joel C -- Shilatifard, Ali -- CA R01CA089455/CA/NCI NIH HHS/ -- R01 CA089455/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2014 Aug 29;345(6200):1065-70. doi: 10.1126/science.1255104.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stowers Institute for Medical Research, 1000 East 50th Street, Kansas City, MO 64110, USA. ; Saint Louis University School of Medicine, Edward A. Doisy Department of Biochemistry and Molecular Biology, St. Louis, MO, USA. ; Stowers Institute for Medical Research, 1000 East 50th Street, Kansas City, MO 64110, USA. Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS 66160, USA. ; Stowers Institute for Medical Research, 1000 East 50th Street, Kansas City, MO 64110, USA. ash@northwestern.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25170156" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Substitution ; Animals ; Chromatin/*metabolism ; Disease Models, Animal ; Drosophila Proteins/genetics ; Drosophila melanogaster ; Gene Silencing ; Glioma/genetics/metabolism ; Heterochromatin/metabolism ; Histone-Lysine N-Methyltransferase/genetics ; Histones/*genetics/metabolism ; Jumonji Domain-Containing Histone Demethylases/metabolism ; Lysine/*genetics ; Methionine/*genetics ; Methylation ; Mutation ; Signal Transduction
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  • 60
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-04-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Buckley, Ralf -- New York, N.Y. -- Science. 2014 Apr 25;344(6182):358. doi: 10.1126/science.344.6182.358-b.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Environment, Griffith University, Gold Coast, QLD 4222, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24763570" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Endangered Species ; *Extinction, Biological ; *Lemur ; Male
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  • 61
    Publication Date: 2014-03-22
    Description: Humans can discriminate several million different colors and almost half a million different tones, but the number of discriminable olfactory stimuli remains unknown. The lay and scientific literature typically claims that humans can discriminate 10,000 odors, but this number has never been empirically validated. We determined the resolution of the human sense of smell by testing the capacity of humans to discriminate odor mixtures with varying numbers of shared components. On the basis of the results of psychophysical testing, we calculated that humans can discriminate at least 1 trillion olfactory stimuli. This is far more than previous estimates of distinguishable olfactory stimuli. It demonstrates that the human olfactory system, with its hundreds of different olfactory receptors, far outperforms the other senses in the number of physically different stimuli it can discriminate.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4483192/" 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/PMC4483192/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bushdid, C -- Magnasco, M O -- Vosshall, L B -- Keller, A -- UL1 TR000043/TR/NCATS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Mar 21;343(6177):1370-2. doi: 10.1126/science.1249168.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Neurogenetics and Behavior, The Rockefeller University, 1230 York Avenue, Box 63, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24653035" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Female ; Humans ; Male ; Middle Aged ; *Odors ; *Olfactory Perception ; Smell/*physiology ; Young Adult
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  • 62
    Publication Date: 2014-05-03
    Description: We demonstrate a technique for mapping brain activity that combines molecular specificity and spatial coverage using a neurotransmitter sensor detectable by magnetic resonance imaging (MRI). This molecular functional MRI (fMRI) method yielded time-resolved volumetric measurements of dopamine release evoked by reward-related lateral hypothalamic brain stimulation of rats injected with the neurotransmitter sensor. Peak dopamine concentrations and release rates were observed in the anterior nucleus accumbens core. Substantial dopamine transients were also present in more caudal areas. Dopamine-release amplitudes correlated with the rostrocaudal stimulation coordinate, suggesting participation of hypothalamic circuitry in modulating dopamine responses. This work provides a foundation for development and application of quantitative molecular fMRI techniques targeted toward numerous components of neural physiology.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Taekwan -- Cai, Lili X -- Lelyveld, Victor S -- Hai, Aviad -- Jasanoff, Alan -- DP2-OD002114/OD/NIH HHS/ -- R01-DA02899/DA/NIDA NIH HHS/ -- R01-NS076462/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2014 May 2;344(6183):533-5. doi: 10.1126/science.1249380.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Engineering, Massachusetts Institute of Technology (MIT), Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24786083" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Proteins/*chemistry/genetics ; Brain Mapping/*methods ; Contrast Media/*chemistry ; Cytochrome P-450 Enzyme System/*chemistry/genetics ; Dopamine/*metabolism ; Dopaminergic Neurons ; Magnetic Resonance Imaging/*methods ; Male ; Molecular Imaging/*methods ; NADPH-Ferrihemoprotein Reductase/*chemistry/genetics ; Nucleus Accumbens/*metabolism ; Rats ; Rats, Sprague-Dawley
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  • 63
    Publication Date: 2014-07-12
    Description: Heterosexual transmission of HIV-1 typically results in one genetic variant establishing systemic infection. We compared, for 137 linked transmission pairs, the amino acid sequences encoded by non-envelope genes of viruses in both partners and demonstrate a selection bias for transmission of residues that are predicted to confer increased in vivo fitness on viruses in the newly infected, immunologically naive recipient. Although tempered by transmission risk factors, such as donor viral load, genital inflammation, and recipient gender, this selection bias provides an overall transmission advantage for viral quasispecies that are dominated by viruses with high in vivo fitness. Thus, preventative or therapeutic approaches that even marginally reduce viral fitness may lower the overall transmission rates and offer long-term benefits even upon successful transmission.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4289910/" 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/PMC4289910/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carlson, Jonathan M -- Schaefer, Malinda -- Monaco, Daniela C -- Batorsky, Rebecca -- Claiborne, Daniel T -- Prince, Jessica -- Deymier, Martin J -- Ende, Zachary S -- Klatt, Nichole R -- DeZiel, Charles E -- Lin, Tien-Ho -- Peng, Jian -- Seese, Aaron M -- Shapiro, Roger -- Frater, John -- Ndung'u, Thumbi -- Tang, Jianming -- Goepfert, Paul -- Gilmour, Jill -- Price, Matt A -- Kilembe, William -- Heckerman, David -- Goulder, Philip J R -- Allen, Todd M -- Allen, Susan -- Hunter, Eric -- 2P51RR000165-51/RR/NCRR NIH HHS/ -- G108/626/Medical Research Council/United Kingdom -- OD P51OD11132/OD/NIH HHS/ -- P01-AI074415/AI/NIAID NIH HHS/ -- P30 AI050409/AI/NIAID NIH HHS/ -- P51 OD010425/OD/NIH HHS/ -- P51 OD011132/OD/NIH HHS/ -- P51RR165/RR/NCRR NIH HHS/ -- R01 AI064060/AI/NIAID NIH HHS/ -- R01 AI64060/AI/NIAID NIH HHS/ -- R37 AI051231/AI/NIAID NIH HHS/ -- R37 AI51231/AI/NIAID NIH HHS/ -- T32 AI007387/AI/NIAID NIH HHS/ -- T32-AI007387/AI/NIAID NIH HHS/ -- U01 AI 66454/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Jul 11;345(6193):1254031. doi: 10.1126/science.1254031. Epub 2014 Jul 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Microsoft Research, Redmond, WA 98052, USA. carlson@microsoft.com ehunte4@emory.edu. ; Emory Vaccine Center at Yerkes National Primate Research Center, Emory University, Atlanta, GA 30329, USA. ; Ragon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology and Harvard University, Cambridge, MA 02114, USA. ; Microsoft Research, Redmond, WA 98052, USA. ; Division of Infectious Diseases, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA. ; Nuffield Department of Clinical Medicine, University of Oxford, Oxford OX1 7BN, UK. National Institute of Health Research, Oxford Biomedical Research Centre, Oxford OX3 7LE, UK. Oxford Martin School, University of Oxford, Oxford OX1 3BD, UK. ; Ragon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology and Harvard University, Cambridge, MA 02114, USA. HIV Pathogenesis Programme, Doris Duke Medical Research Institute, Nelson R. Mandela School of Medicine, University of KwaZulu-Natal, Durban 4013, South Africa. KwaZulu-Natal Research Institute for Tuberculosis and HIV (K-RITH), Nelson R. Mandela School of Medicine, University of KwaZulu-Natal, Durban 4001, South Africa. Max Planck Institute for Infection Biology, D-10117 Berlin, Germany. ; Department of Medicine, University of Alabama at Birmingham, Birmingham, AL 35294, USA. ; International AIDS Vaccine Initiative, London SW10 9NH, UK. Imperial College of Science Technology and Medicine, London SW10 9NH, UK. ; International AIDS Vaccine Initiative, San Francisco, CA 94105, USA. Department of Epidemiology and Biostatistics, University of California, San Francisco, San Francisco, CA 94105, USA. ; Rwanda-Zambia HIV Research Group: Zambia-Emory HIV Research Project, Lusaka, Zambia. ; Microsoft Research, Los Angeles, CA 98117, USA. ; HIV Pathogenesis Programme, Doris Duke Medical Research Institute, Nelson R. Mandela School of Medicine, University of KwaZulu-Natal, Durban 4013, South Africa. Department of Paediatrics, University of Oxford, Oxford OX1 3SY, UK. ; Rwanda-Zambia HIV Research Group: Zambia-Emory HIV Research Project, Lusaka, Zambia. Department of Pathology and Laboratory Medicine, Emory University, Atlanta, GA 30322, USA. Department of Global Health, Rollins School of Public Health, Emory University, Atlanta, GA 30322, USA. ; International AIDS Vaccine Initiative, San Francisco, CA 94105, USA. Microsoft Research, Los Angeles, CA 98117, USA. Department of Paediatrics, University of Oxford, Oxford OX1 3SY, UK. ; Emory Vaccine Center at Yerkes National Primate Research Center, Emory University, Atlanta, GA 30329, USA. Rwanda-Zambia HIV Research Group: Zambia-Emory HIV Research Project, Lusaka, Zambia. Department of Pathology and Laboratory Medicine, Emory University, Atlanta, GA 30322, USA. carlson@microsoft.com ehunte4@emory.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25013080" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Consensus Sequence ; DNA Mutational Analysis ; Disease Transmission, Infectious/statistics & numerical data ; Female ; HIV Infections/*transmission ; HIV-1/*genetics ; *Heterosexuality ; High-Throughput Nucleotide Sequencing ; Human Immunodeficiency Virus Proteins/genetics ; Humans ; Male ; Models, Statistical ; Molecular Sequence Data ; Point Mutation ; Risk Factors ; *Selection, Genetic ; Viral Load
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  • 64
    Publication Date: 2014-01-18
    Description: A major evolutionary transition to eusociality with reproductive division of labor between queens and workers has arisen independently at least 10 times in the ants, bees, and wasps. Pheromones produced by queens are thought to play a key role in regulating this complex social system, but their evolutionary history remains unknown. Here, we identify the first sterility-inducing queen pheromones in a wasp, bumblebee, and desert ant and synthesize existing data on compounds that characterize female fecundity in 64 species of social insects. Our results show that queen pheromones are strikingly conserved across at least three independent origins of eusociality, with wasps, ants, and some bees all appearing to use nonvolatile, saturated hydrocarbons to advertise fecundity and/or suppress worker reproduction. These results suggest that queen pheromones evolved from conserved signals of solitary ancestors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Van Oystaeyen, Annette -- Oliveira, Ricardo Caliari -- Holman, Luke -- van Zweden, Jelle S -- Romero, Carmen -- Oi, Cintia A -- d'Ettorre, Patrizia -- Khalesi, Mohammadreza -- Billen, Johan -- Wackers, Felix -- Millar, Jocelyn G -- Wenseleers, Tom -- New York, N.Y. -- Science. 2014 Jan 17;343(6168):287-90. doi: 10.1126/science.1244899.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Socioecology and Social Evolution, Zoological Institute, University of Leuven, Naamsestraat 59-Box 2466, 3000 Leuven, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24436417" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ants/*physiology ; Bees/*physiology ; Biological Assay ; *Biological Evolution ; Female ; Fertility/drug effects/*physiology ; Male ; Pheromones/classification/pharmacology/*physiology ; Reproduction/drug effects/physiology ; Wasps/*physiology
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  • 65
    Publication Date: 2014-04-05
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4414116/" 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/PMC4414116/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fauci, Anthony S -- Marovich, Mary A -- Dieffenbach, Carl W -- Hunter, Eric -- Buchbinder, Susan P -- P51 OD011132/OD/NIH HHS/ -- P51 RR000165/RR/NCRR NIH HHS/ -- U19 AI096187/AI/NIAID NIH HHS/ -- UM1 AI068614/AI/NIAID NIH HHS/ -- Z01 AI000390-25/Intramural NIH HHS/ -- Z01 AI000677-15/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2014 Apr 4;344(6179):49-51. doi: 10.1126/science.1250672.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24700849" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS Vaccines/*administration & dosage/*immunology/*therapeutic use ; Female ; HIV Antigens/*immunology ; HIV Infections/*immunology/*prevention & control ; HIV-1/*immunology ; Humans ; Male ; T-Lymphocytes/*immunology
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  • 66
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-06-21
    Description: It is not just a manner of speaking: "Mind reading," or working out what others are thinking and feeling, is markedly similar to print reading. Both of these distinctly human skills recover meaning from signs, depend on dedicated cortical areas, are subject to genetically heritable disorders, show cultural variation around a universal core, and regulate how people behave. But when it comes to development, the evidence is conflicting. Some studies show that, like learning to read print, learning to read minds is a long, hard process that depends on tuition. Others indicate that even very young, nonliterate infants are already capable of mind reading. Here, we propose a resolution to this conflict. We suggest that infants are equipped with neurocognitive mechanisms that yield accurate expectations about behavior ("automatic" or "implicit" mind reading), whereas "explicit" mind reading, like literacy, is a culturally inherited skill; it is passed from one generation to the next by verbal instruction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heyes, Cecilia M -- Frith, Chris D -- 091593/Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2014 Jun 20;344(6190):1243091. doi: 10.1126/science.1243091.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉All Souls College and Department of Experimental Psychology, University of Oxford, Oxford OX1 4AL, UK. cecilia.heyes@all-souls.ox.ac.uk. ; Wellcome Trust Centre for Neuroimaging, University College London, London WC1N 3BG, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24948740" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Autistic Disorder/psychology ; Brain/physiology ; Child, Preschool ; Cognition ; *Cultural Evolution ; Dyslexia/psychology ; Female ; Humans ; Learning ; Male ; *Nonverbal Communication ; *Telepathy ; *Theory of Mind
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  • 67
    Publication Date: 2014-05-17
    Description: Neural circuits are shaped by elimination of early-formed redundant synapses during postnatal development. Retrograde signaling from postsynaptic cells regulates synapse elimination. In this work, we identified semaphorins, a family of versatile cell recognition molecules, as retrograde signals for elimination of redundant climbing fiber to Purkinje cell synapses in developing mouse cerebellum. Knockdown of Sema3A, a secreted semaphorin, in Purkinje cells or its receptor in climbing fibers accelerated synapse elimination during postnatal day 8 (P8) to P18. Conversely, knockdown of Sema7A, a membrane-anchored semaphorin, in Purkinje cells or either of its two receptors in climbing fibers impaired synapse elimination after P15. The effect of Sema7A involves signaling by metabotropic glutamate receptor 1, a canonical pathway for climbing fiber synapse elimination. These findings define how semaphorins retrogradely regulate multiple processes of synapse elimination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Uesaka, Naofumi -- Uchigashima, Motokazu -- Mikuni, Takayasu -- Nakazawa, Takanobu -- Nakao, Harumi -- Hirai, Hirokazu -- Aiba, Atsu -- Watanabe, Masahiko -- Kano, Masanobu -- New York, N.Y. -- Science. 2014 May 30;344(6187):1020-3. doi: 10.1126/science.1252514. Epub 2014 May 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurophysiology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-0033, Japan. ; Department of Anatomy, Hokkaido University Graduate School of Medicine, Sapporo 060-8638, Japan. ; Laboratory of Animal Resources, Center for Disease Biology and Integrated Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo 113-0033, Japan. ; Department of Neurophysiology, Gunma University Graduate School of Medicine, Maebashi, Gunma 371-8511, Japan. ; Department of Neurophysiology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-0033, Japan. mkano-tky@m.u-tokyo.ac.jp.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24831527" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/genetics/*metabolism ; Brain/*growth & development/metabolism ; Gene Knockdown Techniques ; Mice ; Mice, Inbred C57BL ; Purkinje Cells/metabolism/*physiology ; RNA Interference ; Rats ; Rats, Sprague-Dawley ; Receptors, Metabotropic Glutamate/genetics/metabolism ; Semaphorin-3A/genetics/*metabolism ; Semaphorins/genetics/*metabolism ; Signal Transduction ; Synapses/genetics/*physiology
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  • 68
    Publication Date: 2014-04-26
    Description: Mutations in the mitochondrial genome are associated with multiple diseases and biological processes; however, little is known about the extent of sequence variation in the mitochondrial transcriptome. By ultra-deeply sequencing mitochondrial RNA (〉6000x) from the whole blood of ~1000 individuals from the CARTaGENE project, we identified remarkable levels of sequence variation within and across individuals, as well as sites that show consistent patterns of posttranscriptional modification. Using a genome-wide association study, we find that posttranscriptional modification of functionally important sites in mitochondrial transfer RNAs (tRNAs) is under strong genetic control, largely driven by a missense mutation in MRPP3 that explains ~22% of the variance. These results reveal a major nuclear genetic determinant of posttranscriptional modification in mitochondria and suggest that tRNA posttranscriptional modification may affect cellular energy production.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hodgkinson, Alan -- Idaghdour, Youssef -- Gbeha, Elias -- Grenier, Jean-Christophe -- Hip-Ki, Elodie -- Bruat, Vanessa -- Goulet, Jean-Philippe -- de Malliard, Thibault -- Awadalla, Philip -- New York, N.Y. -- Science. 2014 Apr 25;344(6182):413-5. doi: 10.1126/science.1251110.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CHU Sainte-Justine Research Centre, Department of Pediatrics, Faculty of Medicine, Universite de Montreal, 3175 Chemin de la Cote-Sainte-Catherine, Montreal, Quebec H3T 1C5, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24763589" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Base Sequence ; DNA, Mitochondrial/chemistry/genetics ; Female ; *Genetic Variation ; *Genome, Mitochondrial ; Genome-Wide Association Study ; High-Throughput Nucleotide Sequencing ; Humans ; Male ; Methylation ; Middle Aged ; Mutation, Missense ; Polymorphism, Single Nucleotide ; RNA/chemistry/*genetics/metabolism ; RNA Processing, Post-Transcriptional ; RNA, Transfer/chemistry/*genetics/metabolism ; Ribonuclease P/*genetics/metabolism ; Sequence Analysis, DNA ; Sequence Analysis, RNA ; Transcriptome
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 69
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-09-13
    Description: The science of morality has drawn heavily on well-controlled but artificial laboratory settings. To study everyday morality, we repeatedly assessed moral or immoral acts and experiences in a large (N = 1252) sample using ecological momentary assessment. Moral experiences were surprisingly frequent and manifold. Liberals and conservatives emphasized somewhat different moral dimensions. Religious and nonreligious participants did not differ in the likelihood or quality of committed moral and immoral acts. Being the target of moral or immoral deeds had the strongest impact on happiness, whereas committing moral or immoral deeds had the strongest impact on sense of purpose. Analyses of daily dynamics revealed evidence for both moral contagion and moral licensing. In sum, morality science may benefit from a closer look at the antecedents, dynamics, and consequences of everyday moral experience.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hofmann, Wilhelm -- Wisneski, Daniel C -- Brandt, Mark J -- Skitka, Linda J -- New York, N.Y. -- Science. 2014 Sep 12;345(6202):1340-3. doi: 10.1126/science.1251560. Epub 2014 Sep 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, University of Cologne, 50931 Cologne, Germany. wilhelm.hofmann@uni-koeln.de. ; Department of Psychology, University of Illinois, Chicago, IL 60607, USA. ; Department of Social Psychology, Tilburg University, 5000, Tilburg, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25214626" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aged ; Employee Discipline ; Female ; Happiness ; Humans ; Male ; Middle Aged ; *Morals ; Personnel Loyalty ; Young Adult
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 70
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-05-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Underwood, Emily -- New York, N.Y. -- Science. 2014 May 23;344(6186):829-31. doi: 10.1126/science.344.6186.829.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24855255" target="_blank"〉PubMed〈/a〉
    Keywords: Age Factors ; Cardiovascular Diseases/mortality ; Cause of Death/*trends ; Female ; Great Britain/epidemiology ; Health/statistics & numerical data/*trends ; *Hierarchy, Social ; Humans ; Male ; Poverty/statistics & numerical data/trends ; Risk Factors ; *Social Class ; Socioeconomic Factors ; Stress, Psychological/etiology
    Print ISSN: 0036-8075
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  • 71
    Publication Date: 2014-03-08
    Description: To systematically investigate the impact of immune stimulation upon regulatory variant activity, we exposed primary monocytes from 432 healthy Europeans to interferon-gamma (IFN-gamma) or differing durations of lipopolysaccharide and mapped expression quantitative trait loci (eQTLs). More than half of cis-eQTLs identified, involving hundreds of genes and associated pathways, are detected specifically in stimulated monocytes. Induced innate immune activity reveals multiple master regulatory trans-eQTLs including the major histocompatibility complex (MHC), coding variants altering enzyme and receptor function, an IFN-beta cytokine network showing temporal specificity, and an interferon regulatory factor 2 (IRF2) transcription factor-modulated network. Induced eQTL are significantly enriched for genome-wide association study loci, identifying context-specific associations to putative causal genes including CARD9, ATM, and IRF8. Thus, applying pathophysiologically relevant immune stimuli assists resolution of functional genetic variants.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4064786/" 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/PMC4064786/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fairfax, Benjamin P -- Humburg, Peter -- Makino, Seiko -- Naranbhai, Vivek -- Wong, Daniel -- Lau, Evelyn -- Jostins, Luke -- Plant, Katharine -- Andrews, Robert -- McGee, Chris -- Knight, Julian C -- 074318/Wellcome Trust/United Kingdom -- 088891/Wellcome Trust/United Kingdom -- 090532/Wellcome Trust/United Kingdom -- 090532/Z/09/Z/Wellcome Trust/United Kingdom -- 281824/European Research Council/International -- 98082/Medical Research Council/United Kingdom -- G1001708/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2014 Mar 7;343(6175):1246949. doi: 10.1126/science.1246949.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Centre for Human Genetics, University of Oxford, Roosevelt Drive, Oxford OX3 7BN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24604202" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Antigens, CD14/immunology ; Aryl Hydrocarbon Hydroxylases/genetics ; Basic-Leucine Zipper Transcription Factors/genetics ; CARD Signaling Adaptor Proteins/genetics ; Chromosome Mapping ; Crohn Disease/epidemiology/*genetics ; Cytochrome P-450 CYP1B1 ; Female ; Gene Expression Regulation/*immunology ; *Genetic Predisposition to Disease ; Genetic Variation ; Genome-Wide Association Study ; Humans ; Immunity, Innate/*genetics ; Indoleamine-Pyrrole 2,3,-Dioxygenase/genetics ; Interferon Regulatory Factor-2/genetics ; Interferon Regulatory Factors/genetics ; Interferon-gamma/pharmacology ; Male ; Middle Aged ; Monocytes/drug effects/*immunology ; Polymorphism, Single Nucleotide ; Quantitative Trait Loci ; Receptors, Purinergic P2/genetics ; Young Adult
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  • 72
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-01-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Capel, Blanche -- R37 HD039963/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2014 Jan 3;343(6166):32-3. doi: 10.1126/science.1248486.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24385621" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Eukaryotic Initiation Factor-2/*physiology ; Female ; Humans ; Male ; *Reproductive Techniques, Assisted ; Sex Determination Processes/*genetics ; Sex-Determining Region Y Protein/*physiology ; Y Chromosome/*genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 73
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-10-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carbone, Francis R -- Gebhardt, Thomas -- New York, N.Y. -- Science. 2014 Oct 3;346(6205):40-1. doi: 10.1126/science.1259925. Epub 2014 Oct 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, The University of Melbourne at The Peter Doherty Institute for Infection and Immunity, The University of Melbourne, Parkville, VIC 3010, Australia. f.carbone@microbiology.unimelb.edu.au. ; Department of Microbiology and Immunology, The University of Melbourne at The Peter Doherty Institute for Infection and Immunity, The University of Melbourne, Parkville, VIC 3010, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25278601" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptive Immunity/*immunology ; Animals ; CD4-Positive T-Lymphocytes/*immunology ; CD8-Positive T-Lymphocytes/*immunology ; Chemokines/*immunology ; Female ; Herpes Genitalis/*immunology ; *Herpesvirus 2, Human ; Immunity, Innate/*immunology ; Immunologic Memory/*immunology ; Macrophages/*immunology ; Male ; Skin/*immunology ; Vagina/*immunology ; Virus Diseases/*immunology
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  • 74
    Publication Date: 2014-10-04
    Description: Human mitochondrial ribosomes are highly divergent from all other known ribosomes and are specialized to exclusively translate membrane proteins. They are linked with hereditary mitochondrial diseases and are often the unintended targets of various clinically useful antibiotics. Using single-particle cryogenic electron microscopy, we have determined the structure of its large subunit to 3.4 angstrom resolution, revealing 48 proteins, 21 of which are specific to mitochondria. The structure unveils an adaptation of the exit tunnel for hydrophobic nascent peptides, extensive remodeling of the central protuberance, including recruitment of mitochondrial valine transfer RNA (tRNA(Val)) to play an integral structural role, and changes in the tRNA binding sites related to the unusual characteristics of mitochondrial tRNAs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4246062/" 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/PMC4246062/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, Alan -- Amunts, Alexey -- Bai, Xiao-chen -- Sugimoto, Yoichiro -- Edwards, Patricia C -- Murshudov, Garib -- Scheres, Sjors H W -- Ramakrishnan, V -- 096570/Wellcome Trust/United Kingdom -- MC_U105184332/Medical Research Council/United Kingdom -- MC_UP_A025_1012/Medical Research Council/United Kingdom -- MC_UP_A025_1013/Medical Research Council/United Kingdom -- WT096570/Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2014 Nov 7;346(6210):718-22. doi: 10.1126/science.1258026. Epub 2014 Oct 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council, Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge CB2 0QH, UK. ; Medical Research Council, Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge CB2 0QH, UK. ramak@mrc-lmb.cam.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25278503" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites ; Cryoelectron Microscopy ; Humans ; Mitochondria/genetics/*metabolism ; Mitochondrial Proteins/chemistry/ultrastructure ; Mutation ; Nucleic Acid Conformation ; Protein Conformation ; RNA, Transfer, Val/analysis/*chemistry ; Ribosome Subunits/*chemistry/genetics/*ultrastructure
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  • 75
    Publication Date: 2014-02-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moss-Racusin, Corinne A -- van der Toorn, Jojanneke -- Dovidio, John F -- Brescoll, Victoria L -- Graham, Mark J -- Handelsman, Jo -- 1R13GM090574-01/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Feb 7;343(6171):615-6. doi: 10.1126/science.1245936.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Skidmore College, Saratoga Springs, NY 12866, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24503840" target="_blank"〉PubMed〈/a〉
    Keywords: *Cultural Diversity ; Female ; Humans ; Male ; *Racism ; Research Design ; Science/ethics/*manpower ; *Sexism
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  • 76
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-11-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Underwood, Emily -- New York, N.Y. -- Science. 2014 Oct 31;346(6209):568-71. doi: 10.1126/science.346.6209.568.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25359963" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Aging/*physiology ; Brain/*growth & development ; Child ; Female ; Humans ; *Intelligence Tests ; Male ; Population Dynamics ; Scotland
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  • 77
    Publication Date: 2014-05-31
    Description: Phosphatidylinositol 4-kinases (PI4Ks) and small guanosine triphosphatases (GTPases) are essential for processes that require expansion and remodeling of phosphatidylinositol 4-phosphate (PI4P)-containing membranes, including cytokinesis, intracellular development of malarial pathogens, and replication of a wide range of RNA viruses. However, the structural basis for coordination of PI4K, GTPases, and their effectors is unknown. Here, we describe structures of PI4Kbeta (PI4KIIIbeta) bound to the small GTPase Rab11a without and with the Rab11 effector protein FIP3. The Rab11-PI4KIIIbeta interface is distinct compared with known structures of Rab complexes and does not involve switch regions used by GTPase effectors. Our data provide a mechanism for how PI4KIIIbeta coordinates Rab11 and its effectors on PI4P-enriched membranes and also provide strategies for the design of specific inhibitors that could potentially target plasmodial PI4KIIIbeta to combat malaria.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4046302/" 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/PMC4046302/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burke, John E -- Inglis, Alison J -- Perisic, Olga -- Masson, Glenn R -- McLaughlin, Stephen H -- Rutaganira, Florentine -- Shokat, Kevan M -- Williams, Roger L -- MC_U105184308/Medical Research Council/United Kingdom -- PG/11/109/29247/British Heart Foundation/United Kingdom -- PG11/109/29247/British Heart Foundation/United Kingdom -- R01AI099245/AI/NIAID NIH HHS/ -- T32 GM064337/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 May 30;344(6187):1035-8. doi: 10.1126/science.1253397.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council (MRC) Laboratory of Molecular Biology, Cambridge CB2 0QH, UK. jeburke@uvic.ca rlw@mrc-lmb.cam.ac.uk. ; Medical Research Council (MRC) Laboratory of Molecular Biology, Cambridge CB2 0QH, UK. ; Howard Hughes Medical Institute and Department of Cellular and Molecular Pharmacology, University of California, San Francisco (UCSF), San Francisco, CA 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24876499" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antimalarials/chemistry/pharmacology ; Binding Sites ; Cell Line ; Crystallography, X-Ray ; Drug Design ; Humans ; I-kappa B Kinase/*chemistry ; Molecular Sequence Data ; Mutation ; Phosphotransferases (Alcohol Group Acceptor)/*chemistry/genetics ; Plasmodium/drug effects/growth & development ; Protein Binding ; Protein Structure, Secondary ; Protein Structure, Tertiary ; rab GTP-Binding Proteins/*chemistry
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  • 78
    Publication Date: 2014-01-05
    Description: Decapentaplegic (Dpp), a Drosophila morphogen signaling protein, transfers directly at synapses made at sites of contact between cells that produce Dpp and cytonemes that extend from recipient cells. The Dpp that cytonemes receive moves together with activated receptors toward the recipient cell body in motile puncta. Genetic loss-of-function conditions for diaphanous, shibire, neuroglian, and capricious perturbed cytonemes by reducing their number or only the synapses they make with cells they target, and reduced cytoneme-mediated transport of Dpp and Dpp signaling. These experiments provide direct evidence that cells use cytonemes to exchange signaling proteins, that cytoneme-based exchange is essential for signaling and normal development, and that morphogen distribution and signaling can be contact-dependent, requiring cytoneme synapses.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4336149/" 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/PMC4336149/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roy, Sougata -- Huang, Hai -- Liu, Songmei -- Kornberg, Thomas B -- GM030637/GM/NIGMS NIH HHS/ -- K99HL114867/HL/NHLBI NIH HHS/ -- R01 GM030637/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2014 Feb 21;343(6173):1244624. doi: 10.1126/science.1244624. Epub 2014 Jan 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cardiovascular Research Institute, University of California, San Francisco, CA 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24385607" target="_blank"〉PubMed〈/a〉
    Keywords: Air Sacs/cytology/metabolism ; Animals ; Carrier Proteins/genetics/metabolism ; Cell Adhesion Molecules, Neuronal/genetics/metabolism ; *Cell Communication ; Drosophila Proteins/genetics/*metabolism ; Drosophila melanogaster/*cytology/*metabolism ; Dynamins/genetics/metabolism ; Membrane Proteins/genetics/metabolism ; Protein Transport ; Pseudopodia/*metabolism ; Signal Transduction ; Trachea/cytology/metabolism
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  • 79
    Publication Date: 2014-03-08
    Description: Little is known about how human genetic variation affects the responses to environmental stimuli in the context of complex diseases. Experimental and computational approaches were applied to determine the effects of genetic variation on the induction of pathogen-responsive genes in human dendritic cells. We identified 121 common genetic variants associated in cis with variation in expression responses to Escherichia coli lipopolysaccharide, influenza, or interferon-beta (IFN-beta). We localized and validated causal variants to binding sites of pathogen-activated STAT (signal transducer and activator of transcription) and IRF (IFN-regulatory factor) transcription factors. We also identified a common variant in IRF7 that is associated in trans with type I IFN induction in response to influenza infection. Our results reveal common alleles that explain interindividual variation in pathogen sensing and provide functional annotation for genetic variants that alter susceptibility to inflammatory diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4124741/" 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/PMC4124741/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Mark N -- Ye, Chun -- Villani, Alexandra-Chloe -- Raj, Towfique -- Li, Weibo -- Eisenhaure, Thomas M -- Imboywa, Selina H -- Chipendo, Portia I -- Ran, F Ann -- Slowikowski, Kamil -- Ward, Lucas D -- Raddassi, Khadir -- McCabe, Cristin -- Lee, Michelle H -- Frohlich, Irene Y -- Hafler, David A -- Kellis, Manolis -- Raychaudhuri, Soumya -- Zhang, Feng -- Stranger, Barbara E -- Benoist, Christophe O -- De Jager, Philip L -- Regev, Aviv -- Hacohen, Nir -- DP1 CA174427/CA/NCI NIH HHS/ -- DP1 MH100706/DP/NCCDPHP CDC HHS/ -- DP1 MH100706/MH/NIMH NIH HHS/ -- DP2 OD002230/OD/NIH HHS/ -- F32 AG043267/AG/NIA NIH HHS/ -- P30 DK043351/DK/NIDDK NIH HHS/ -- P50 HG006193/HG/NHGRI NIH HHS/ -- R01 AI091568/AI/NIAID NIH HHS/ -- R01 AR063759/AR/NIAMS NIH HHS/ -- R01 DK097768/DK/NIDDK NIH HHS/ -- R01 HG004037/HG/NHGRI NIH HHS/ -- RC2 GM093080/GM/NIGMS NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- T32 HG002295/HG/NHGRI NIH HHS/ -- U19 AI082630/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Mar 7;343(6175):1246980. doi: 10.1126/science.1246980.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Broad Institute of Massachusetts Institute of Technology (MIT) and Harvard, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24604203" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Autoimmune Diseases/genetics ; Communicable Diseases/genetics ; Dendritic Cells/drug effects/*immunology ; Escherichia coli ; Female ; *Gene-Environment Interaction ; Genetic Loci ; Genome-Wide Association Study ; HEK293 Cells ; Host-Pathogen Interactions/*genetics ; Humans ; Influenza A virus ; Interferon Regulatory Factor-7/*genetics ; Interferon-beta/pharmacology ; Lipopolysaccharides/immunology ; Male ; Middle Aged ; Polymorphism, Single Nucleotide ; Quantitative Trait Loci ; STAT Transcription Factors/*genetics ; Transcriptome ; Young Adult
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  • 80
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-08-16
    Description: Parenting behaviors, such as the provisioning of food by parents to offspring, are known to be highly responsive to changes in environment. However, we currently know little about how such flexibility affects the ways in which parenting is adapted and evolves in response to environmental variation. This is because few studies quantify how individuals vary in their response to changing environments, especially social environments created by other individuals with which parents interact. Social environmental factors differ from nonsocial factors, such as food availability, because parents and offspring both contribute and respond to the social environment they experience. This interdependence leads to the coevolution of flexible behaviors involved in parenting, which could, paradoxically, constrain the ability of individuals to rapidly adapt to changes in their nonsocial environment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Royle, Nick J -- Russell, Andrew F -- Wilson, Alastair J -- BB/G022976/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- New York, N.Y. -- Science. 2014 Aug 15;345(6198):776-81. doi: 10.1126/science.1253294. Epub 2014 Aug 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Ecology and Conservation, College of Life and Environmental Sciences, University of Exeter, Cornwall Campus, Penryn TR10 9EZ, UK. n.j.royle@exeter.ac.uk. ; Centre for Ecology and Conservation, College of Life and Environmental Sciences, University of Exeter, Cornwall Campus, Penryn TR10 9EZ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25124432" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Biological ; Animals ; *Biological Evolution ; Environment ; Female ; Male ; *Maternal Behavior ; *Parenting ; *Paternal Behavior ; Social Environment
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  • 81
    Publication Date: 2014-01-25
    Description: Canine transmissible venereal tumor (CTVT) is the oldest known somatic cell lineage. It is a transmissible cancer that propagates naturally in dogs. We sequenced the genomes of two CTVT tumors and found that CTVT has acquired 1.9 million somatic substitution mutations and bears evidence of exposure to ultraviolet light. CTVT is remarkably stable and lacks subclonal heterogeneity despite thousands of rearrangements, copy-number changes, and retrotransposon insertions. More than 10,000 genes carry nonsynonymous variants, and 646 genes have been lost. CTVT first arose in a dog with low genomic heterozygosity that may have lived about 11,000 years ago. The cancer spawned by this individual dispersed across continents about 500 years ago. Our results provide a genetic identikit of an ancient dog and demonstrate the robustness of mammalian somatic cells to survive for millennia despite a massive mutation burden.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3918581/" 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/PMC3918581/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Murchison, Elizabeth P -- Wedge, David C -- Alexandrov, Ludmil B -- Fu, Beiyuan -- Martincorena, Inigo -- Ning, Zemin -- Tubio, Jose M C -- Werner, Emma I -- Allen, Jan -- De Nardi, Andrigo Barboza -- Donelan, Edward M -- Marino, Gabriele -- Fassati, Ariberto -- Campbell, Peter J -- Yang, Fengtang -- Burt, Austin -- Weiss, Robin A -- Stratton, Michael R -- 088340/Wellcome Trust/United Kingdom -- 098051/Wellcome Trust/United Kingdom -- G0501446/Medical Research Council/United Kingdom -- G0900950/Medical Research Council/United Kingdom -- G9721629/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2014 Jan 24;343(6169):437-40. doi: 10.1126/science.1247167.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Sanger Institute, Hinxton CB10 1SA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24458646" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Lineage/*genetics ; Dog Diseases/*genetics ; Dogs/*genetics ; Founder Effect ; Gene Dosage ; Genome ; Karyotype ; Mutation ; Retroelements ; Venereal Tumors, Veterinary/*epidemiology/*genetics
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  • 82
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-03-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Underwood, Emily -- New York, N.Y. -- Science. 2014 Feb 28;343(6174):964-7. doi: 10.1126/science.343.6174.964.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24578561" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Brain/drug effects/metabolism/pathology ; Child ; Chromosomes, Human, Pair 21/genetics ; Clinical Trials as Topic ; Cognition Disorders/*drug therapy ; Down Syndrome/drug therapy/genetics/*therapy ; *Early Medical Intervention ; Female ; GABA Antagonists/therapeutic use ; Humans ; Magnetic Resonance Imaging ; Male ; Mice ; Mutagenesis, Insertional ; Picrotoxin/therapeutic use ; RNA, Long Noncoding/genetics ; gamma-Aminobutyric Acid/metabolism
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  • 83
    Publication Date: 2014-01-05
    Description: Pregnenolone is considered the inactive precursor of all steroid hormones, and its potential functional effects have been largely uninvestigated. The administration of the main active principle of Cannabis sativa (marijuana), Delta(9)-tetrahydrocannabinol (THC), substantially increases the synthesis of pregnenolone in the brain via activation of the type-1 cannabinoid (CB1) receptor. Pregnenolone then, acting as a signaling-specific inhibitor of the CB1 receptor, reduces several effects of THC. This negative feedback mediated by pregnenolone reveals a previously unknown paracrine/autocrine loop protecting the brain from CB1 receptor overactivation that could open an unforeseen approach for the treatment of cannabis intoxication and addiction.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4057431/" 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/PMC4057431/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vallee, Monique -- Vitiello, Sergio -- Bellocchio, Luigi -- Hebert-Chatelain, Etienne -- Monlezun, Stephanie -- Martin-Garcia, Elena -- Kasanetz, Fernando -- Baillie, Gemma L -- Panin, Francesca -- Cathala, Adeline -- Roullot-Lacarriere, Valerie -- Fabre, Sandy -- Hurst, Dow P -- Lynch, Diane L -- Shore, Derek M -- Deroche-Gamonet, Veronique -- Spampinato, Umberto -- Revest, Jean-Michel -- Maldonado, Rafael -- Reggio, Patricia H -- Ross, Ruth A -- Marsicano, Giovanni -- Piazza, Pier Vincenzo -- 260515/European Research Council/International -- DA-003934/DA/NIDA NIH HHS/ -- DA-03672/DA/NIDA NIH HHS/ -- DA-09789/DA/NIDA NIH HHS/ -- K05 DA021358/DA/NIDA NIH HHS/ -- R01 DA003934/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2014 Jan 3;343(6166):94-8. doi: 10.1126/science.1243985.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INSERM, Neurocentre Magendie, Physiopathologie de la Plasticite Neuronale, U862, F-33000 Bordeaux, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24385629" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*drug effects/metabolism ; Cannabinoid Receptor Antagonists/administration & dosage ; Cannabis/*toxicity ; Dronabinol/*toxicity ; Male ; Marijuana Abuse/drug therapy ; Mice ; Mice, Inbred C57BL ; Pregnenolone/*administration & dosage/*metabolism ; Rats ; Rats, Sprague-Dawley ; Rats, Wistar ; Receptor, Cannabinoid, CB1/*agonists/*antagonists & inhibitors
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  • 84
    Publication Date: 2014-03-29
    Description: In many metazoans, germ cells are separated from somatic lineages early in development and maintain their identity throughout life. Here, we show that a Polycomb group (PcG) component, Enhancer of Zeste [E(z)], a histone transferase that generates trimethylation at lysine 27 of histone H3, maintains germline identity in Drosophila adult testes. We find excessive early-stage somatic gonadal cells in E(z) mutant testes, which originate from both overproliferative cyst stem cells and germ cells turning on an early-stage somatic cell marker. Using complementary lineage-tracing experiments in E(z) mutant testes, a portion of excessive early-stage somatic gonadal cells are found to originate from early-stage germ cells, including germline stem cells. Moreover, knocking down E(z) specifically in somatic cells caused this change, which suggests a non-cell autonomous role of E(z) to antagonize somatic identity in germ cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4040133/" 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/PMC4040133/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eun, Suk Ho -- Shi, Zhen -- Cui, Kairong -- Zhao, Keji -- Chen, Xin -- R00 HD055052/HD/NICHD NIH HHS/ -- R00HD055052/HD/NICHD NIH HHS/ -- R01 HD065816/HD/NICHD NIH HHS/ -- R01HD065816/HD/NICHD NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2014 Mar 28;343(6178):1513-6. doi: 10.1126/science.1246514.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, The Johns Hopkins University, Baltimore, MD 21218, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24675960" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomarkers/metabolism ; Cell Differentiation ; Cell Lineage ; Drosophila Proteins/genetics/*physiology ; Drosophila melanogaster/cytology/*growth & development ; Male ; Nuclear Proteins/genetics/*physiology ; Polycomb Repressive Complex 2/genetics/*physiology ; Spermatocytes ; Spermatogonia/*metabolism ; Testis/cytology/*growth & development
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  • 85
    Publication Date: 2014-03-29
    Description: High-quality early childhood programs have been shown to have substantial benefits in reducing crime, raising earnings, and promoting education. Much less is known about their benefits for adult health. We report on the long-term health effects of one of the oldest and most heavily cited early childhood interventions with long-term follow-up evaluated by the method of randomization: the Carolina Abecedarian Project (ABC). Using recently collected biomedical data, we find that disadvantaged children randomly assigned to treatment have significantly lower prevalence of risk factors for cardiovascular and metabolic diseases in their mid-30s. The evidence is especially strong for males. The mean systolic blood pressure among the control males is 143 millimeters of mercury (mm Hg), whereas it is only 126 mm Hg among the treated. One in four males in the control group is affected by metabolic syndrome, whereas none in the treatment group are affected. To reach these conclusions, we address several statistical challenges. We use exact permutation tests to account for small sample sizes and conduct a parallel bootstrap confidence interval analysis to confirm the permutation analysis. We adjust inference to account for the multiple hypotheses tested and for nonrandom attrition. Our evidence shows the potential of early life interventions for preventing disease and promoting health.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4028126/" 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/PMC4028126/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Campbell, Frances -- Conti, Gabriella -- Heckman, James J -- Moon, Seong Hyeok -- Pinto, Rodrigo -- Pungello, Elizabeth -- Pan, Yi -- 1R01HD54702/HD/NICHD NIH HHS/ -- 5R37HD065072/HD/NICHD NIH HHS/ -- 5RC1MD004344/MD/NIMHD NIH HHS/ -- R37 HD065072/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2014 Mar 28;343(6178):1478-85. doi: 10.1126/science.1248429.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Frank Porter Graham Child Development Institute, University of North Carolina, Chapel Hill, NC 27599, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24675955" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Biomarkers/blood ; Blood Preservation ; Body Mass Index ; Cardiovascular Diseases/*epidemiology/physiopathology/*prevention & control ; Child ; Cholesterol, HDL/blood ; Diet ; Early Medical Intervention/*methods ; Female ; Health ; Humans ; Male ; Metabolic Syndrome X/*epidemiology/physiopathology/*prevention & control
    Print ISSN: 0036-8075
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  • 86
    Publication Date: 2014-03-22
    Description: Avian brood parasites lay eggs in the nests of other birds, which raise the unrelated chicks and typically suffer partial or complete loss of their own brood. However, carrion crows Corvus corone corone can benefit from parasitism by the great spotted cuckoo Clamator glandarius. Parasitized nests have lower rates of predation-induced failure due to production of a repellent secretion by cuckoo chicks, but among nests that are successful, those with cuckoo chicks fledge fewer crows. The outcome of these counterbalancing effects fluctuates between parasitism and mutualism each season, depending on the intensity of predation pressure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Canestrari, Daniela -- Bolopo, Diana -- Turlings, Ted C J -- Roder, Gregory -- Marcos, Jose M -- Baglione, Vittorio -- New York, N.Y. -- Science. 2014 Mar 21;343(6177):1350-2. doi: 10.1126/science.1249008.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology of Organisms and Systems, University of Oviedo, Oviedo, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24653032" target="_blank"〉PubMed〈/a〉
    Keywords: Acids/analysis/metabolism ; Animals ; Birds/growth & development/*physiology ; Bodily Secretions/chemistry ; Crows/growth & development/*physiology ; Female ; Indoles/analysis/metabolism ; Male ; *Nesting Behavior ; Phenols/analysis/metabolism ; Predatory Behavior ; Reproduction ; Sulfur Compounds/analysis/metabolism ; *Symbiosis ; Volatilization
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  • 87
    Publication Date: 2014-08-16
    Description: The current view of motor learning suggests that when we revisit a task, the brain recalls the motor commands it previously learned. In this view, motor memory is a memory of motor commands, acquired through trial-and-error and reinforcement. Here we show that the brain controls how much it is willing to learn from the current error through a principled mechanism that depends on the history of past errors. This suggests that the brain stores a previously unknown form of memory, a memory of errors. A mathematical formulation of this idea provides insights into a host of puzzling experimental data, including savings and meta-learning, demonstrating that when we are better at a motor task, it is partly because the brain recognizes the errors it experienced before.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4506639/" 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/PMC4506639/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Herzfeld, David J -- Vaswani, Pavan A -- Marko, Mollie K -- Shadmehr, Reza -- 1F31NS079121/NS/NINDS NIH HHS/ -- F31 NS090860/NS/NINDS NIH HHS/ -- R01 NS078311/NS/NINDS NIH HHS/ -- R01NS078311/NS/NINDS NIH HHS/ -- T32 GM007309/GM/NIGMS NIH HHS/ -- T32EB003383/EB/NIBIB NIH HHS/ -- T32GM007057/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2014 Sep 12;345(6202):1349-53. doi: 10.1126/science.1253138. Epub 2014 Aug 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biomedical Engineering, Laboratory for Computational Motor Control, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. dherzfe1@jhmi.edu. ; Department of Neuroscience, Laboratory for Computational Motor Control, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. ; Department of Biomedical Engineering, Laboratory for Computational Motor Control, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25123484" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Brain/*physiology ; Female ; Humans ; Learning/*physiology ; Male ; Mental Recall/*physiology ; *Psychomotor Performance ; Young Adult
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  • 88
    Publication Date: 2014-03-15
    Description: Motor neurons, which relay neural commands to drive skeletal muscle movements, encompass types ranging from "slow" to "fast," whose biophysical properties govern the timing, gradation, and amplitude of muscle force. Here we identify the noncanonical Notch ligand Delta-like homolog 1 (Dlk1) as a determinant of motor neuron functional diversification. Dlk1, expressed by ~30% of motor neurons, is necessary and sufficient to promote a fast biophysical signature in the mouse and chick. Dlk1 suppresses Notch signaling and activates expression of the K(+) channel subunit Kcng4 to modulate delayed-rectifier currents. Dlk1 inactivation comprehensively shifts motor neurons toward slow biophysical and transcriptome signatures, while abolishing peak force outputs. Our findings provide insights into the development of motor neuron functional diversity and its contribution to the execution of movements.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Muller, Daniel -- Cherukuri, Pitchaiah -- Henningfeld, Kristine -- Poh, Chor Hoon -- Wittler, Lars -- Grote, Phillip -- Schluter, Oliver -- Schmidt, Jennifer -- Laborda, Jorge -- Bauer, Steven R -- Brownstone, Robert M -- Marquardt, Till -- R01 HD042013/HD/NICHD NIH HHS/ -- Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2014 Mar 14;343(6176):1264-6. doi: 10.1126/science.1246448.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Developmental Neurobiology Laboratory, European Neuroscience Institute (ENI-G), Grisebachstrasse 5, 37077 Gottingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24626931" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Gene Expression Regulation ; Intercellular Signaling Peptides and Proteins/genetics/*physiology ; Mice ; Mice, Knockout ; Motor Neurons/*metabolism ; Movement ; Muscle Fibers, Skeletal/physiology ; Muscle, Skeletal/innervation/*physiology ; Potassium Channels, Voltage-Gated/genetics ; Receptors, Notch/*physiology ; Signal Transduction ; Transcriptome
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  • 89
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-09-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Enserink, Martin -- New York, N.Y. -- Science. 2014 Sep 12;345(6202):1261. doi: 10.1126/science.345.6202.1261.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25214602" target="_blank"〉PubMed〈/a〉
    Keywords: Accidents, Traffic/*mortality ; Child ; Child, Preschool ; Female ; Head Protective Devices/*utilization ; Humans ; Male ; Motorcycles/*legislation & jurisprudence ; Vietnam/epidemiology ; Wounds and Injuries/mortality/*prevention & control
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 90
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-06-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Euston, David R -- Steenland, Hendrik W -- New York, N.Y. -- Science. 2014 Jun 6;344(6188):1087-8. doi: 10.1126/science.1255649.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Canadian Centre for Behavioral Neuroscience, University of Lethbridge, Lethbridge, Alberta T1K 3M4, Canada. david.euston@gmail.com. ; Canadian Centre for Behavioral Neuroscience, University of Lethbridge, Lethbridge, Alberta T1K 3M4, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24904140" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dendritic Spines/*physiology ; Female ; Learning/*physiology ; Male ; Motor Cortex/*physiology ; Sleep, REM/*physiology
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  • 91
    Publication Date: 2014-04-05
    Description: Adrenal Cushing's syndrome is caused by excess production of glucocorticoid from adrenocortical tumors and hyperplasias, which leads to metabolic disorders. We performed whole-exome sequencing of 49 blood-tumor pairs and RNA sequencing of 44 tumors from cortisol-producing adrenocortical adenomas (ACAs), adrenocorticotropic hormone-independent macronodular adrenocortical hyperplasias (AIMAHs), and adrenocortical oncocytomas (ADOs). We identified a hotspot in the PRKACA gene with a L205R mutation in 69.2% (27 out of 39) of ACAs and validated in 65.5% of a total of 87 ACAs. Our data revealed that the activating L205R mutation, which locates in the P+1 loop of the protein kinase A (PKA) catalytic subunit, promoted PKA substrate phosphorylation and target gene expression. Moreover, we discovered the recurrently mutated gene DOT1L in AIMAHs and CLASP2 in ADOs. Collectively, these data highlight potentially functional mutated genes in adrenal Cushing's syndrome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cao, Yanan -- He, Minghui -- Gao, Zhibo -- Peng, Ying -- Li, Yanli -- Li, Lin -- Zhou, Weiwei -- Li, Xiangchun -- Zhong, Xu -- Lei, Yiming -- Su, Tingwei -- Wang, Hang -- Jiang, Yiran -- Yang, Lin -- Wei, Wei -- Yang, Xu -- Jiang, Xiuli -- Liu, Li -- He, Juan -- Ye, Junna -- Wei, Qing -- Li, Yingrui -- Wang, Weiqing -- Wang, Jun -- Ning, Guang -- New York, N.Y. -- Science. 2014 May 23;344(6186):913-7. doi: 10.1126/science.1249480. Epub 2014 Apr 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Shanghai Clinical Center for Endocrine and Metabolic Diseases, Shanghai Key Laboratory for Endocrine Tumors, Rui-Jin Hospital, Shanghai Jiao-Tong University School of Medicine, Shanghai, China. ; BGI-Shanghai, BGI-Shenzhen, Shenzhen, China. ; Department of Pathology, Rui-Jin Hospital, Shanghai Jiao-Tong University School of Medicine, Shanghai, China. ; Shanghai Clinical Center for Endocrine and Metabolic Diseases, Shanghai Key Laboratory for Endocrine Tumors, Rui-Jin Hospital, Shanghai Jiao-Tong University School of Medicine, Shanghai, China. guangning@medmail.com.cn wangj@genomics.org.cn wqingw@hotmail.com. ; BGI-Shanghai, BGI-Shenzhen, Shenzhen, China. Department of Biology, University of Copenhagen, Copenhagen, Denmark. King Abdulaziz University, Jeddah, Saudi Arabia. Macau University of Science and Technology, Macau, China. Department of Medicine, University of Hong Kong, Hong Kong. guangning@medmail.com.cn wangj@genomics.org.cn wqingw@hotmail.com. ; Shanghai Clinical Center for Endocrine and Metabolic Diseases, Shanghai Key Laboratory for Endocrine Tumors, Rui-Jin Hospital, Shanghai Jiao-Tong University School of Medicine, Shanghai, China. Laboratory of Endocrinology and Metabolism, Institute of Health Sciences, Shanghai Institutes for Biological Sciences (SIBS), Chinese Academy of Sciences (CAS), and Shanghai Jiao Tong University School of Medicine (SJTUSM), Shanghai, China. guangning@medmail.com.cn wangj@genomics.org.cn wqingw@hotmail.com.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24700472" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Cortex Neoplasms/*genetics/*metabolism ; Adrenocortical Adenoma/*genetics/*metabolism ; Amino Acid Substitution ; Arginine/genetics ; Catalytic Domain/genetics ; Cells, Cultured ; Cushing Syndrome/*genetics ; Cyclic AMP-Dependent Protein Kinase Catalytic Subunits/chemistry/*genetics ; Glucocorticoids/metabolism ; Humans ; Hydrocortisone/*metabolism ; Leucine/genetics ; Methyltransferases/genetics ; Microtubule-Associated Proteins/genetics ; Mutation
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  • 92
    Publication Date: 2014-07-12
    Description: This paper presents a new data infrastructure for measuring economic activity. The infrastructure records transactions and account balances, yielding measurements with scope and accuracy that have little precedent in economics. The data are drawn from a diverse population that overrepresents males and younger adults but contains large numbers of underrepresented groups. The data infrastructure permits evaluation of a benchmark theory in economics that predicts that individuals should use a combination of cash management, saving, and borrowing to make the timing of income irrelevant for the timing of spending. As in previous studies and in contrast to the predictions of the theory, there is a response of spending to the arrival of anticipated income. The data also show, however, that this apparent excess sensitivity of spending results largely from the coincident timing of regular income and regular spending. The remaining excess sensitivity is concentrated among individuals with less liquidity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gelman, Michael -- Kariv, Shachar -- Shapiro, Matthew D -- Silverman, Dan -- Tadelis, Steven -- P30 AG012839/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2014 Jul 11;345(6193):212-5. doi: 10.1126/science.1247727.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Economics, University of Michigan, Ann Arbor, MI 48109, USA. ; Department of Economics, University of California, Berkeley, Berkeley, CA 94720, USA. ; Department of Economics, University of Michigan, Ann Arbor, MI 48109, USA. National Bureau of Economic Research (NBER), Cambridge, MA 02138, USA. shapiro@umich.edu. ; National Bureau of Economic Research (NBER), Cambridge, MA 02138, USA. Department of Economics, Arizona State University, Tempe, AZ 85287, USA. ; National Bureau of Economic Research (NBER), Cambridge, MA 02138, USA. Haas School of Business, University of California, Berkeley, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25013075" target="_blank"〉PubMed〈/a〉
    Keywords: Administrative Personnel ; Adolescent ; Adult ; Aged ; Female ; *Human Activities ; Humans ; *Income ; Male ; Middle Aged ; Policy Making ; Young Adult
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  • 93
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-10-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, David A -- New York, N.Y. -- Science. 2014 Oct 3;346(6205):134. doi: 10.1126/science.346.6205.134. Epub 2014 Oct 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉David Anderson is a Ph.D. student and NSF Graduate Research Fellow at Washington University in St. Louis. For more on life and careers, visit www.sciencecareers.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25278613" target="_blank"〉PubMed〈/a〉
    Keywords: *Career Choice ; Emigration and Immigration/legislation & jurisprudence ; *Homosexuality, Male ; Human Rights/*legislation & jurisprudence ; Humans ; *Love ; Male ; Marine Biology ; Marriage/*legislation & jurisprudence
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 94
    Publication Date: 2014-05-31
    Description: A substantial literature shows that U.S. early childhood interventions have important long-term economic benefits. However, there is little evidence on this question for developing countries. We report substantial effects on the earnings of participants in a randomized intervention conducted in 1986-1987 that gave psychosocial stimulation to growth-stunted Jamaican toddlers. The intervention consisted of weekly visits from community health workers over a 2-year period that taught parenting skills and encouraged mothers and children to interact in ways that develop cognitive and socioemotional skills. The authors reinterviewed 105 out of 129 study participants 20 years later and found that the intervention increased earnings by 25%, enough for them to catch up to the earnings of a nonstunted comparison group identified at baseline (65 out of 84 participants).〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4574862/" 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/PMC4574862/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gertler, Paul -- Heckman, James -- Pinto, Rodrigo -- Zanolini, Arianna -- Vermeersch, Christel -- Walker, Susan -- Chang, Susan M -- Grantham-McGregor, Sally -- R01 HD054702/HD/NICHD NIH HHS/ -- R01HD54702/HD/NICHD NIH HHS/ -- R37 HD065072/HD/NICHD NIH HHS/ -- R37HD065072/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2014 May 30;344(6187):998-1001. doi: 10.1126/science.1251178.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of California Berkeley, Berkeley, CA, USA. National Bureau of Economic Research (NBER), Cambridge, MA, USA. gertler@haas.berkeley.edu. ; University of Chicago, Chicago, IL, USA. American Bar Foundation, Chicago, IL, USA. Institute for Fiscal Studies, University College London, London, UK. ; University of Chicago, Chicago, IL, USA. ; The World Bank, Washington, DC, USA. ; The University of The West Indies, Kingston, Jamaica. ; University College London, London, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24876490" target="_blank"〉PubMed〈/a〉
    Keywords: *Child Development ; Child, Preschool ; Cognition ; Developing Countries/*statistics & numerical data ; Early Intervention (Education)/*statistics & numerical data ; Emotions ; Employment/*economics/trends ; Female ; Humans ; Infant ; Jamaica ; Male ; Mother-Child Relations/*psychology ; Parenting/psychology ; Psychology ; Salaries and Fringe Benefits/*statistics & numerical data ; Young Adult
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  • 95
    Publication Date: 2014-01-11
    Description: It has been assumed that most, if not all, signals regulating early development have been identified. Contrary to this expectation, we identified 28 candidate signaling proteins expressed during zebrafish embryogenesis, including Toddler, a short, conserved, and secreted peptide. Both absence and overproduction of Toddler reduce the movement of mesendodermal cells during zebrafish gastrulation. Local and ubiquitous production of Toddler promote cell movement, suggesting that Toddler is neither an attractant nor a repellent but acts globally as a motogen. Toddler drives internalization of G protein-coupled APJ/Apelin receptors, and activation of APJ/Apelin signaling rescues toddler mutants. These results indicate that Toddler is an activator of APJ/Apelin receptor signaling, promotes gastrulation movements, and might be the first in a series of uncharacterized developmental signals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4107353/" 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/PMC4107353/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pauli, Andrea -- Norris, Megan L -- Valen, Eivind -- Chew, Guo-Liang -- Gagnon, James A -- Zimmerman, Steven -- Mitchell, Andrew -- Ma, Jiao -- Dubrulle, Julien -- Reyon, Deepak -- Tsai, Shengdar Q -- Joung, J Keith -- Saghatelian, Alan -- Schier, Alexander F -- K99 HD076935/HD/NICHD NIH HHS/ -- R01 GM056211/GM/NIGMS NIH HHS/ -- R01 GM102491/GM/NIGMS NIH HHS/ -- R01 HG005111/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Feb 14;343(6172):1248636. doi: 10.1126/science.1248636. Epub 2014 Jan 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24407481" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Cell Movement ; Chemokine CXCL12/metabolism ; Frameshift Mutation ; Gastrulation/genetics/*physiology ; Molecular Sequence Data ; Receptors, G-Protein-Coupled/genetics/*metabolism ; Signal Transduction ; Zebrafish/*embryology/genetics/metabolism ; Zebrafish Proteins/genetics/*metabolism
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  • 96
    Publication Date: 2014-03-29
    Description: Rapid advances in DNA synthesis techniques have made it possible to engineer viruses, biochemical pathways and assemble bacterial genomes. Here, we report the synthesis of a functional 272,871-base pair designer eukaryotic chromosome, synIII, which is based on the 316,617-base pair native Saccharomyces cerevisiae chromosome III. Changes to synIII include TAG/TAA stop-codon replacements, deletion of subtelomeric regions, introns, transfer RNAs, transposons, and silent mating loci as well as insertion of loxPsym sites to enable genome scrambling. SynIII is functional in S. cerevisiae. Scrambling of the chromosome in a heterozygous diploid reveals a large increase in a-mater derivatives resulting from loss of the MATalpha allele on synIII. The complete design and synthesis of synIII establishes S. cerevisiae as the basis for designer eukaryotic genome biology.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4033833/" 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/PMC4033833/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Annaluru, Narayana -- Muller, Heloise -- Mitchell, Leslie A -- Ramalingam, Sivaprakash -- Stracquadanio, Giovanni -- Richardson, Sarah M -- Dymond, Jessica S -- Kuang, Zheng -- Scheifele, Lisa Z -- Cooper, Eric M -- Cai, Yizhi -- Zeller, Karen -- Agmon, Neta -- Han, Jeffrey S -- Hadjithomas, Michalis -- Tullman, Jennifer -- Caravelli, Katrina -- Cirelli, Kimberly -- Guo, Zheyuan -- London, Viktoriya -- Yeluru, Apurva -- Murugan, Sindurathy -- Kandavelou, Karthikeyan -- Agier, Nicolas -- Fischer, Gilles -- Yang, Kun -- Martin, J Andrew -- Bilgel, Murat -- Bohutski, Pavlo -- Boulier, Kristin M -- Capaldo, Brian J -- Chang, Joy -- Charoen, Kristie -- Choi, Woo Jin -- Deng, Peter -- DiCarlo, James E -- Doong, Judy -- Dunn, Jessilyn -- Feinberg, Jason I -- Fernandez, Christopher -- Floria, Charlotte E -- Gladowski, David -- Hadidi, Pasha -- Ishizuka, Isabel -- Jabbari, Javaneh -- Lau, Calvin Y L -- Lee, Pablo A -- Li, Sean -- Lin, Denise -- Linder, Matthias E -- Ling, Jonathan -- Liu, Jaime -- Liu, Jonathan -- London, Mariya -- Ma, Henry -- Mao, Jessica -- McDade, Jessica E -- McMillan, Alexandra -- Moore, Aaron M -- Oh, Won Chan -- Ouyang, Yu -- Patel, Ruchi -- Paul, Marina -- Paulsen, Laura C -- Qiu, Judy -- Rhee, Alex -- Rubashkin, Matthew G -- Soh, Ina Y -- Sotuyo, Nathaniel E -- Srinivas, Venkatesh -- Suarez, Allison -- Wong, Andy -- Wong, Remus -- Xie, Wei Rose -- Xu, Yijie -- Yu, Allen T -- Koszul, Romain -- Bader, Joel S -- Boeke, Jef D -- Chandrasegaran, Srinivasan -- 092076/Wellcome Trust/United Kingdom -- GM077291/GM/NIGMS NIH HHS/ -- R01 GM077291/GM/NIGMS NIH HHS/ -- R01 GM090192/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2014 Apr 4;344(6179):55-8. doi: 10.1126/science.1249252. Epub 2014 Mar 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Environmental Health Sciences, Johns Hopkins University (JHU) School of Public Health, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24674868" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; *Chromosomes, Fungal/genetics/metabolism ; DNA, Fungal/genetics ; Genes, Fungal ; Genetic Fitness ; Genome, Fungal ; Genomic Instability ; Introns ; Molecular Sequence Data ; Mutation ; Polymerase Chain Reaction ; RNA, Fungal/genetics ; RNA, Transfer/genetics ; Saccharomyces cerevisiae/cytology/*genetics/physiology ; Sequence Analysis, DNA ; Sequence Deletion ; Synthetic Biology/*methods ; Transformation, Genetic
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  • 97
    Publication Date: 2014-12-17
    Description: Songbirds represent an important model organism for elucidating molecular mechanisms that link genes with complex behaviors, in part because they have discrete vocal learning circuits that have parallels with those that mediate human speech. We found that ~10% of the genes in the avian genome were regulated by singing, and we found a striking regional diversity of both basal and singing-induced programs in the four key song nuclei of the zebra finch, a vocal learning songbird. The region-enriched patterns were a result of distinct combinations of region-enriched transcription factors (TFs), their binding motifs, and presinging acetylation of histone 3 at lysine 27 (H3K27ac) enhancer activity in the regulatory regions of the associated genes. RNA interference manipulations validated the role of the calcium-response transcription factor (CaRF) in regulating genes preferentially expressed in specific song nuclei in response to singing. Thus, differential combinatorial binding of a small group of activity-regulated TFs and predefined epigenetic enhancer activity influences the anatomical diversity of behaviorally regulated gene networks.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4359888/" 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/PMC4359888/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Whitney, Osceola -- Pfenning, Andreas R -- Howard, Jason T -- Blatti, Charles A -- Liu, Fang -- Ward, James M -- Wang, Rui -- Audet, Jean-Nicoles -- Kellis, Manolis -- Mukherjee, Sayan -- Sinha, Saurabh -- Hartemink, Alexander J -- West, Anne E -- Jarvis, Erich D -- 5T32MH018882-18/MH/NIMH NIH HHS/ -- R01 DC007218/DC/NIDCD NIH HHS/ -- R01 HG004037/HG/NHGRI NIH HHS/ -- R01DC007218/DC/NIDCD NIH HHS/ -- R21 NS084336/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Dec 12;346(6215):1256780. doi: 10.1126/science.1256780.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Howard Hughes Medical Institute, and Duke University Medical Center, Durham, NC 27710, USA. owhitney@gmail.com apfenning@csail.mit.edu west@neuro.duke.edu jarvis@neuro.duke.edu. ; Department of Neurobiology, Howard Hughes Medical Institute, and Duke University Medical Center, Durham, NC 27710, USA. Computer Science and Artificial Intelligence Laboratory and the Broad Institute of MIT and Harvard, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. owhitney@gmail.com apfenning@csail.mit.edu west@neuro.duke.edu jarvis@neuro.duke.edu. ; Department of Neurobiology, Howard Hughes Medical Institute, and Duke University Medical Center, Durham, NC 27710, USA. ; Department of Computer Science, University of Illinois, Urbana-Champaign, IL, USA. ; Department of Neurobiology, Duke University Medical Center, Durham, NC 27710, USA. ; Department of Biology, McGill University, Montreal, Quebec H3A 1B1, Canada. ; Computer Science and Artificial Intelligence Laboratory and the Broad Institute of MIT and Harvard, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. ; Department of Statistics, Duke University, Durham, NC, USA. ; Department of Computer Science, Duke University, Durham, NC 27708-0129, USA. ; Department of Neurobiology, Duke University Medical Center, Durham, NC 27710, USA. owhitney@gmail.com apfenning@csail.mit.edu west@neuro.duke.edu jarvis@neuro.duke.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25504732" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Avian Proteins/chemistry/genetics/metabolism ; Brain/*physiology ; Enhancer Elements, Genetic ; Epigenesis, Genetic ; Finches/*genetics/*physiology ; *Gene Expression Regulation ; *Gene Regulatory Networks ; Genome ; Histones/metabolism ; Male ; Regulatory Sequences, Nucleic Acid ; Transcription Factors/chemistry/genetics/metabolism ; *Transcriptome ; *Vocalization, Animal
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  • 98
    Publication Date: 2014-02-22
    Description: Robustness, the maintenance of a character in the presence of genetic change, can help preserve adaptive traits but also may hinder evolvability, the ability to bring forth novel adaptations. We used genotype networks to analyze the binding site repertoires of 193 transcription factors from mice and yeast, providing empirical evidence that robustness and evolvability need not be conflicting properties. Network vertices represent binding sites where two sites are connected if they differ in a single nucleotide. We show that the binding sites of larger genotype networks are not only more robust, but the sequences adjacent to such networks can also bind more transcription factors, thus demonstrating that robustness can facilitate evolvability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Payne, Joshua L -- Wagner, Andreas -- New York, N.Y. -- Science. 2014 Feb 21;343(6173):875-7. doi: 10.1126/science.1249046.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Zurich, Institute of Evolutionary Biology and Environmental Studies, Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24558158" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Binding Sites/genetics ; Gene Regulatory Networks ; Mice ; Mutation ; Saccharomyces cerevisiae Proteins/chemistry ; Transcription Factors/*chemistry ; Transcription, Genetic
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  • 99
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-05-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, Jocelyn -- New York, N.Y. -- Science. 2014 May 16;344(6185):687-9. doi: 10.1126/science.344.6185.687.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24833372" target="_blank"〉PubMed〈/a〉
    Keywords: Actinin/genetics ; Animals ; Caspase 12/genetics ; *Gene Knockout Techniques ; *Genetic Association Studies ; Humans ; Mice ; *Molecular Targeted Therapy ; Muscular Dystrophies/genetics ; Mutation ; NAV1.7 Voltage-Gated Sodium Channel/genetics ; Proprotein Convertases/genetics ; Receptors, CCR5/genetics ; Serine Endopeptidases/genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 100
    Publication Date: 2014-10-18
    Description: Small molecules are useful tools for probing the biological function and therapeutic potential of individual proteins, but achieving selectivity is challenging when the target protein shares structural domains with other proteins. The Bromo and Extra-Terminal (BET) proteins have attracted interest because of their roles in transcriptional regulation, epigenetics, and cancer. The BET bromodomains (protein interaction modules that bind acetyl-lysine) have been targeted by potent small-molecule inhibitors, but these inhibitors lack selectivity for individual family members. We developed an ethyl derivative of an existing small-molecule inhibitor, I-BET/JQ1, and showed that it binds leucine/alanine mutant bromodomains with nanomolar affinity and achieves up to 540-fold selectivity relative to wild-type bromodomains. Cell culture studies showed that blockade of the first bromodomain alone is sufficient to displace a specific BET protein, Brd4, from chromatin. Expansion of this approach could help identify the individual roles of single BET proteins in human physiology and disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4458378/" 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/PMC4458378/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baud, Matthias G J -- Lin-Shiao, Enrique -- Cardote, Teresa -- Tallant, Cynthia -- Pschibul, Annica -- Chan, Kwok-Ho -- Zengerle, Michael -- Garcia, Jordi R -- Kwan, Terence T-L -- Ferguson, Fleur M -- Ciulli, Alessio -- 097945/Z/11/Z/Wellcome Trust/United Kingdom -- 100476/Z/12/Z/Wellcome Trust/United Kingdom -- BB/G023123/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/J001201/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- New York, N.Y. -- Science. 2014 Oct 31;346(6209):638-41. doi: 10.1126/science.1249830. Epub 2014 Oct 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biological Chemistry and Drug Discovery, College of Life Sciences, University of Dundee, James Black Centre, Dow Street, Dundee, DD1 5EH, UK. Department of Chemistry, University of Cambridge, Lensfield Road, Cambridge CB2 1EW, UK. ; Division of Biological Chemistry and Drug Discovery, College of Life Sciences, University of Dundee, James Black Centre, Dow Street, Dundee, DD1 5EH, UK. ; Department of Chemistry, University of Cambridge, Lensfield Road, Cambridge CB2 1EW, UK. ; Division of Biological Chemistry and Drug Discovery, College of Life Sciences, University of Dundee, James Black Centre, Dow Street, Dundee, DD1 5EH, UK. Department of Chemistry, University of Cambridge, Lensfield Road, Cambridge CB2 1EW, UK. a.ciulli@dundee.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25323695" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Azepines/chemistry/pharmacology ; Cell Line, Tumor ; Chromatin/chemistry ; Crystallography, X-Ray ; Humans ; Leucine/genetics ; Models, Molecular ; Molecular Probes/*chemistry ; Mutation ; Nuclear Proteins/antagonists & inhibitors/*chemistry/genetics ; Protein Engineering/*methods ; Protein Structure, Tertiary ; Transcription Factors/antagonists & inhibitors/*chemistry/genetics ; Triazoles/chemistry/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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