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  • 1
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    Actin polymerization-driven molecular movement of mDia1 in living cells (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-03-27
    Description: mDia1, a Rho effector, belongs to the Formin family of proteins, which shares the conserved tandem FH1-FH2 unit structure. Formins including mDia1 accelerate actin nucleation while interacting with actin filament fast-growing ends. Here our single-molecule imaging revealed fast directional movement of mDia1 FH1-FH2 for tens of microns in living cells. The movement of mDia1 FH1-FH2 was blocked by actin-perturbing drugs, and the speed of mDia1 FH1-FH2 movement appeared to correlate with actin elongation rates. In vitro, mDia1 FH1-FH2 associated persistently with the growing actin barbed end. mDia1 probably moves processively along the growing end of actin filaments in cells, and Formins may be a molecular motility machinery that is independent from motor proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Higashida, Chiharu -- Miyoshi, Takushi -- Fujita, Akiko -- Oceguera-Yanez, Fabian -- Monypenny, James -- Andou, Yoshikazu -- Narumiya, Shuh -- Watanabe, Naoki -- New York, N.Y. -- Science. 2004 Mar 26;303(5666):2007-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Kyoto University Faculty of Medicine, Yoshida Konoe-cho, Sakyo-ku, Kyoto, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15044801" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/drug effects/*physiology/ultrastructure ; Actins/*metabolism ; Animals ; Bicyclo Compounds, Heterocyclic/metabolism/pharmacology ; Biopolymers ; Carrier Proteins/chemistry/metabolism/*physiology ; Cytochalasin D/metabolism/pharmacology ; *Depsipeptides ; Mice ; Microtubules/drug effects/physiology ; Movement ; Mutation ; Myosins/physiology ; Peptides, Cyclic/pharmacology ; Recombinant Fusion Proteins/chemistry/metabolism ; Thiazoles/metabolism/pharmacology ; Thiazolidines ; Xenopus ; rhoA GTP-Binding Protein/metabolism/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Genome-scale functional characterization of Drosophila developmental enhancers in vivo (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-06-05
    Description: Transcriptional enhancers are crucial regulators of gene expression and animal development and the characterization of their genomic organization, spatiotemporal activities and sequence properties is a key goal in modern biology. Here we characterize the in vivo activity of 7,705 Drosophila melanogaster enhancer candidates covering 13.5% of the non-coding non-repetitive genome throughout embryogenesis. 3,557 (46%) candidates are active, suggesting a high density with 50,000 to 100,000 developmental enhancers genome-wide. The vast majority of enhancers display specific spatial patterns that are highly dynamic during development. Most appear to regulate their neighbouring genes, suggesting that the cis-regulatory genome is organized locally into domains, which are supported by chromosomal domains, insulator binding and genome evolution. However, 12 to 21 per cent of enhancers appear to skip non-expressed neighbours and regulate a more distal gene. Finally, we computationally identify cis-regulatory motifs that are predictive and required for enhancer activity, as we validate experimentally. This work provides global insights into the organization of an animal regulatory genome and the make-up of enhancer sequences and confirms and generalizes principles from previous studies. All enhancer patterns are annotated manually with a controlled vocabulary and all results are available through a web interface (http://enhancers.starklab.org), including the raw images of all microscopy slides for manual inspection at arbitrary zoom levels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kvon, Evgeny Z -- Kazmar, Tomas -- Stampfel, Gerald -- Yanez-Cuna, J Omar -- Pagani, Michaela -- Schernhuber, Katharina -- Dickson, Barry J -- Stark, Alexander -- England -- Nature. 2014 Aug 7;512(7512):91-5. doi: 10.1038/nature13395. Epub 2014 Jun 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Research Institute of Molecular Pathology (IMP), Vienna Biocenter VBC, Dr Bohr-Gasse 7, 1030 Vienna, Austria [2] Howard Hughes Medical Institute, Janelia Farm Research Campus, Ashburn, Virginia 20147, USA (B.J.D.); Genomics Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA (E.Z.K.). ; Research Institute of Molecular Pathology (IMP), Vienna Biocenter VBC, Dr Bohr-Gasse 7, 1030 Vienna, Austria. ; 1] Research Institute of Molecular Pathology (IMP), Vienna Biocenter VBC, Dr Bohr-Gasse 7, 1030 Vienna, Austria [2].〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24896182" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Drosophila melanogaster/*embryology/*genetics ; Embryonic Development/*genetics ; Enhancer Elements, Genetic/*genetics ; Gene Expression Regulation, Developmental/*genetics ; Genome, Insect/*genetics ; Internet ; Nucleotide Motifs/genetics ; Organ Specificity/genetics ; Regulatory Sequences, Nucleic Acid/genetics ; Reproducibility of Results ; User-Computer Interface
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    Conservation. High value and long life--double jeopardy for tunas and billfishes (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-07-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Collette, B B -- Carpenter, K E -- Polidoro, B A -- Juan-Jorda, M J -- Boustany, A -- Die, D J -- Elfes, C -- Fox, W -- Graves, J -- Harrison, L R -- McManus, R -- Minte-Vera, C V -- Nelson, R -- Restrepo, V -- Schratwieser, J -- Sun, C-L -- Amorim, A -- Brick Peres, M -- Canales, C -- Cardenas, G -- Chang, S-K -- Chiang, W-C -- de Oliveira Leite, N Jr -- Harwell, H -- Lessa, R -- Fredou, F L -- Oxenford, H A -- Serra, R -- Shao, K-T -- Sumaila, R -- Wang, S-P -- Watson, R -- Yanez, E -- New York, N.Y. -- Science. 2011 Jul 15;333(6040):291-2. doi: 10.1126/science.1208730. Epub 2011 Jul 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Marine Fisheries Service Systematics Laboratory, National Oceanic and Atmospheric Administration, USA. collettb@si.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21737699" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Conservation of Natural Resources ; *Endangered Species/statistics & numerical data ; Fisheries ; *Perciformes/physiology ; Population Dynamics ; Seafood/economics ; *Tuna/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 4
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    C9orf72 is required for proper macrophage and microglial function in mice (2016)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2016-03-19
    Description: Expansions of a hexanucleotide repeat (GGGGCC) in the noncoding region of the C9orf72 gene are the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. Decreased expression of C9orf72 is seen in expansion carriers, suggesting that loss of function may play a role in disease. We found that two independent mouse lines lacking the C9orf72 ortholog (3110043O21Rik) in all tissues developed normally and aged without motor neuron disease. Instead, C9orf72 null mice developed progressive splenomegaly and lymphadenopathy with accumulation of engorged macrophage-like cells. C9orf72 expression was highest in myeloid cells, and the loss of C9orf72 led to lysosomal accumulation and altered immune responses in macrophages and microglia, with age-related neuroinflammation similar to C9orf72 ALS but not sporadic ALS human patient tissue. Thus, C9orf72 is required for the normal function of myeloid cells, and altered microglial function may contribute to neurodegeneration in C9orf72 expansion carriers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Rourke, J G -- Bogdanik, L -- Yanez, A -- Lall, D -- Wolf, A J -- Muhammad, A K M G -- Ho, R -- Carmona, S -- Vit, J P -- Zarrow, J -- Kim, K J -- Bell, S -- Harms, M B -- Miller, T M -- Dangler, C A -- Underhill, D M -- Goodridge, H S -- Lutz, C M -- Baloh, R H -- GM085796/GM/NIGMS NIH HHS/ -- NS069669/NS/NINDS NIH HHS/ -- NS078398/NS/NINDS NIH HHS/ -- NS087351/NS/NINDS NIH HHS/ -- UL1TR000124/TR/NCATS NIH HHS/ -- New York, N.Y. -- Science. 2016 Mar 18;351(6279):1324-9. doi: 10.1126/science.aaf1064.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Board of Governors Regenerative Medicine Institute, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, CA 90048, USA. ; The Jackson Laboratory, Bar Harbor, ME, USA. ; Division of Biomedical Sciences, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, CA 90048, USA. ; Department of Neurology, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110, USA. ; Board of Governors Regenerative Medicine Institute, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, CA 90048, USA. Department of Neurology, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, CA 90048, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26989253" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/immunology ; Amyotrophic Lateral Sclerosis/genetics/*immunology ; Animals ; Frontotemporal Dementia/genetics/*immunology ; Gene Knockdown Techniques ; Guanine Nucleotide Exchange Factors/genetics/*physiology ; Heterozygote ; Humans ; Lymphatic Diseases/genetics/immunology ; Macrophages/*immunology ; Mice ; Mice, Knockout ; Microglia/*immunology ; Myeloid Cells/*immunology ; Proteins/genetics/*physiology ; Rats ; Splenomegaly/genetics/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 5
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    Daily magnesium fluxes regulate cellular timekeeping and energy balance (2016)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2016-04-14
    Description: Circadian clocks are fundamental to the biology of most eukaryotes, coordinating behaviour and physiology to resonate with the environmental cycle of day and night through complex networks of clock-controlled genes. A fundamental knowledge gap exists, however, between circadian gene expression cycles and the biochemical mechanisms that ultimately facilitate circadian regulation of cell biology. Here we report circadian rhythms in the intracellular concentration of magnesium ions, [Mg(2+)]i, which act as a cell-autonomous timekeeping component to determine key clock properties both in a human cell line and in a unicellular alga that diverged from each other more than 1 billion years ago. Given the essential role of Mg(2+) as a cofactor for ATP, a functional consequence of [Mg(2+)]i oscillations is dynamic regulation of cellular energy expenditure over the daily cycle. Mechanistically, we find that these rhythms provide bilateral feedback linking rhythmic metabolism to clock-controlled gene expression. The global regulation of nucleotide triphosphate turnover by intracellular Mg(2+) availability has potential to impact upon many of the cell's more than 600 MgATP-dependent enzymes and every cellular system where MgNTP hydrolysis becomes rate limiting. Indeed, we find that circadian control of translation by mTOR is regulated through [Mg(2+)]i oscillations. It will now be important to identify which additional biological processes are subject to this form of regulation in tissues of multicellular organisms such as plants and humans, in the context of health and disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Feeney, Kevin A -- Hansen, Louise L -- Putker, Marrit -- Olivares-Yanez, Consuelo -- Day, Jason -- Eades, Lorna J -- Larrondo, Luis F -- Hoyle, Nathaniel P -- O'Neill, John S -- van Ooijen, Gerben -- 093734/Z/10/Z/Wellcome Trust/United Kingdom -- MC_UP_1201/4/Medical Research Council/United Kingdom -- England -- Nature. 2016 Apr 21;532(7599):375-9. doi: 10.1038/nature17407. Epub 2016 Apr 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MRC Laboratory for Molecular Biology, Francis Crick Avenue, Cambridge Biomedical Campus, Cambridge CB2 0QH, UK. ; School of Biological Sciences, University of Edinburgh, Max Born Crescent, Edinburgh EH9 3BF, UK. ; Millennium Nucleus for Fungal Integrative and Synthetic Biology, Departamento de Genetica Molecular y Microbiologia, Facultad de Ciencias Biologicas, Pontificia Universidad Catolica de Chile, Casilla 114-D, Santiago, Chile. ; Department of Earth Sciences, University of Cambridge, Downing Street, Cambridge CB2 3EQ, UK. ; School of Chemistry, University of Edinburgh, David Brewster Road, Edinburgh EH9 3FJ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27074515" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Cell Line ; Chlorophyta/cytology/metabolism ; Circadian Clocks/genetics/*physiology ; Circadian Rhythm/genetics/*physiology ; *Energy Metabolism ; Feedback, Physiological ; Gene Expression Regulation ; Humans ; Intracellular Space/metabolism ; Magnesium/*metabolism ; Male ; Mice ; TOR Serine-Threonine Kinases/metabolism ; Time Factors
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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