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  • Mutation  (99)
  • American Association for the Advancement of Science (AAAS)  (99)
  • 2015-2019
  • 2010-2014  (80)
  • 1980-1984  (19)
  • 2012  (80)
  • 1984  (19)
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  • 2015-2019
  • 2010-2014  (80)
  • 1980-1984  (19)
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  • 1
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    MARF1 regulates essential oogenic processes in mice (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-24
    Description: Development of fertilization-competent oocytes depends on integrated processes controlling meiosis, cytoplasmic development, and maintenance of genomic integrity. We show that meiosis arrest female 1 (MARF1) is required for these processes in mammalian oocytes. Mutations of Marf1 cause female infertility characterized by up-regulation of a cohort of transcripts, increased retrotransposon expression, defective cytoplasmic maturation, and meiotic arrest. Up-regulation of protein phosphatase 2 catalytic subunit (PPP2CB) is key to the meiotic arrest phenotype. Moreover, Iap and Line1 retrotransposon messenger RNAs are also up-regulated, and, concomitantly, DNA double-strand breaks are elevated in mutant oocytes. Therefore MARF1, by suppressing levels of specific transcripts, is an essential regulator of important oogenic processes leading to female fertility and the development of healthy offspring.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3612990/" 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/PMC3612990/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Su, You-Qiang -- Sugiura, Koji -- Sun, Fengyun -- Pendola, Janice K -- Cox, Gregory A -- Handel, Mary Ann -- Schimenti, John C -- Eppig, John J -- CA34196/CA/NCI NIH HHS/ -- HD42137/HD/NICHD NIH HHS/ -- P01 HD042137/HD/NICHD NIH HHS/ -- P30 CA034196/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2012 Mar 23;335(6075):1496-9. doi: 10.1126/science.1214680.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Jackson Laboratory, Bar Harbor, ME 04609, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22442484" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Cycle Proteins/chemistry/genetics/*metabolism ; DNA Breaks, Double-Stranded ; Embryonic Development ; Female ; *Fertility ; Meiosis ; Mice ; Molecular Sequence Data ; Mutation ; Oocytes/*physiology ; *Oogenesis ; Phenotype ; Protein Phosphatase 2/genetics/metabolism ; Protein Structure, Tertiary ; RNA, Messenger/genetics/metabolism ; Retroelements ; Transcription, Genetic ; Transcriptome ; Up-Regulation
    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
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    The ancient drug salicylate directly activates AMP-activated protein kinase (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-04-21
    Description: Salicylate, a plant product, has been in medicinal use since ancient times. More recently, it has been replaced by synthetic derivatives such as aspirin and salsalate, both of which are rapidly broken down to salicylate in vivo. At concentrations reached in plasma after administration of salsalate or of aspirin at high doses, salicylate activates adenosine monophosphate-activated protein kinase (AMPK), a central regulator of cell growth and metabolism. Salicylate binds at the same site as the synthetic activator A-769662 to cause allosteric activation and inhibition of dephosphorylation of the activating phosphorylation site, threonine-172. In AMPK knockout mice, effects of salicylate to increase fat utilization and to lower plasma fatty acids in vivo were lost. Our results suggest that AMPK activation could explain some beneficial effects of salsalate and aspirin in humans.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3399766/" 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/PMC3399766/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hawley, Simon A -- Fullerton, Morgan D -- Ross, Fiona A -- Schertzer, Jonathan D -- Chevtzoff, Cyrille -- Walker, Katherine J -- Peggie, Mark W -- Zibrova, Darya -- Green, Kevin A -- Mustard, Kirsty J -- Kemp, Bruce E -- Sakamoto, Kei -- Steinberg, Gregory R -- Hardie, D Grahame -- 080982/Wellcome Trust/United Kingdom -- 097726/Wellcome Trust/United Kingdom -- MC_U127088492/Medical Research Council/United Kingdom -- Canadian Institutes of Health Research/Canada -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2012 May 18;336(6083):918-22. doi: 10.1126/science.1215327. Epub 2012 Apr 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cell Signalling and Immunology, College of Life Sciences, University of Dundee, Dundee DD1 5EH, Scotland, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22517326" target="_blank"〉PubMed〈/a〉
    Keywords: AMP-Activated Protein Kinases/genetics/*metabolism ; Amino Acid Substitution ; Animals ; Aspirin/pharmacology ; Binding Sites ; Carbohydrate Metabolism/drug effects ; Cell Line ; Enzyme Activation ; Enzyme Activators/pharmacology ; HEK293 Cells ; Humans ; Lipid Metabolism/drug effects ; Liver/drug effects/metabolism ; Mice ; Mice, Knockout ; Mutation ; Oxygen Consumption/drug effects ; Phosphorylation ; Pyrones/pharmacology ; Rats ; Salicylates/blood/*metabolism/*pharmacology ; Thiophenes/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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  • 3
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    Airborne transmission of influenza A/H5N1 virus between ferrets (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-23
    Description: Highly pathogenic avian influenza A/H5N1 virus can cause morbidity and mortality in humans but thus far has not acquired the ability to be transmitted by aerosol or respiratory droplet ("airborne transmission") between humans. To address the concern that the virus could acquire this ability under natural conditions, we genetically modified A/H5N1 virus by site-directed mutagenesis and subsequent serial passage in ferrets. The genetically modified A/H5N1 virus acquired mutations during passage in ferrets, ultimately becoming airborne transmissible in ferrets. None of the recipient ferrets died after airborne infection with the mutant A/H5N1 viruses. Four amino acid substitutions in the host receptor-binding protein hemagglutinin, and one in the polymerase complex protein basic polymerase 2, were consistently present in airborne-transmitted viruses. The transmissible viruses were sensitive to the antiviral drug oseltamivir and reacted well with antisera raised against H5 influenza vaccine strains. Thus, avian A/H5N1 influenza viruses can acquire the capacity for airborne transmission between mammals without recombination in an intermediate host and therefore constitute a risk for human pandemic influenza.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Herfst, Sander -- Schrauwen, Eefje J A -- Linster, Martin -- Chutinimitkul, Salin -- de Wit, Emmie -- Munster, Vincent J -- Sorrell, Erin M -- Bestebroer, Theo M -- Burke, David F -- Smith, Derek J -- Rimmelzwaan, Guus F -- Osterhaus, Albert D M E -- Fouchier, Ron A M -- DP1-OD000490-01/OD/NIH HHS/ -- HHSN266200700010C/PHS HHS/ -- New York, N.Y. -- Science. 2012 Jun 22;336(6088):1534-41. doi: 10.1126/science.1213362.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Virology, Erasmus Medical Center, Rotterdam, The Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22723413" target="_blank"〉PubMed〈/a〉
    Keywords: Air Microbiology ; Amino Acid Substitution ; Animals ; Antiviral Agents/pharmacology ; Containment of Biohazards ; Disease Models, Animal ; Female ; *Ferrets ; Hemagglutinin Glycoproteins, Influenza ; Virus/chemistry/genetics/immunology/metabolism ; Humans ; Immune Sera ; Influenza A Virus, H5N1 Subtype/drug effects/*genetics/*pathogenicity/physiology ; Influenza in Birds/epidemiology/virology ; Influenza, Human/epidemiology/transmission/*virology ; Molecular Sequence Data ; Mutagenesis, Site-Directed ; Mutation ; Orthomyxoviridae Infections/transmission/*virology ; Oseltamivir/pharmacology ; Pandemics ; Poultry ; RNA Replicase/chemistry/genetics ; Reassortant Viruses/pathogenicity ; Receptors, Virus/metabolism ; Respiratory System/*virology ; Reverse Genetics ; Serial Passage ; Sialic Acids/metabolism ; Viral Proteins/chemistry/genetics ; Virulence ; Virus Replication ; Virus Shedding
    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
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    Secreted kinase phosphorylates extracellular proteins that regulate biomineralization (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-05-15
    Description: Protein phosphorylation is a fundamental mechanism regulating nearly every aspect of cellular life. Several secreted proteins are phosphorylated, but the kinases responsible are unknown. We identified a family of atypical protein kinases that localize within the Golgi apparatus and are secreted. Fam20C appears to be the Golgi casein kinase that phosphorylates secretory pathway proteins within S-x-E motifs. Fam20C phosphorylates the caseins and several secreted proteins implicated in biomineralization, including the small integrin-binding ligand, N-linked glycoproteins (SIBLINGs). Consequently, mutations in Fam20C cause an osteosclerotic bone dysplasia in humans known as Raine syndrome. Fam20C is thus a protein kinase dedicated to the phosphorylation of extracellular proteins.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3754843/" 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/PMC3754843/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tagliabracci, Vincent S -- Engel, James L -- Wen, Jianzhong -- Wiley, Sandra E -- Worby, Carolyn A -- Kinch, Lisa N -- Xiao, Junyu -- Grishin, Nick V -- Dixon, Jack E -- DK018024-37/DK/NIDDK NIH HHS/ -- DK018849-36/DK/NIDDK NIH HHS/ -- GM094575/GM/NIGMS NIH HHS/ -- R01 DK018849/DK/NIDDK NIH HHS/ -- R37 DK018024/DK/NIDDK NIH HHS/ -- T32 CA009523/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Jun 1;336(6085):1150-3. doi: 10.1126/science.1217817. Epub 2012 May 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of California, San Diego, La Jolla, CA 92093-0721, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22582013" target="_blank"〉PubMed〈/a〉
    Keywords: Abnormalities, Multiple/genetics/metabolism ; Amino Acid Motifs ; Amino Acid Sequence ; Animals ; Calcification, Physiologic ; Casein Kinase I ; Casein Kinases/metabolism ; Caseins/*metabolism ; Cattle ; Cell Line, Tumor ; Cleft Palate/genetics/metabolism ; Exophthalmos/genetics/metabolism ; Extracellular Matrix Proteins/chemistry/genetics/*metabolism/secretion ; Glycoproteins/metabolism ; Golgi Apparatus/*enzymology ; HEK293 Cells ; HeLa Cells ; Humans ; Microcephaly/genetics/metabolism ; Milk/enzymology ; Molecular Sequence Data ; Mutation ; Osteopontin ; Osteosclerosis/genetics/metabolism ; Phosphorylation ; Protein Sorting Signals ; Recombinant Fusion Proteins/chemistry/metabolism/secretion ; *Secretory Pathway ; Substrate Specificity
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 5
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    Alzheimer's research. How to talk about Alzheimer's risk (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-08-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, Greg -- New York, N.Y. -- Science. 2012 Aug 17;337(6096):792. doi: 10.1126/science.337.6096.792.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22903992" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*diagnosis/*genetics ; Apolipoprotein E4/genetics ; Clinical Trials as Topic ; Genetic Predisposition to Disease ; Humans ; Mutation ; *Patient Selection ; Risk ; Risk Assessment
    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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  • 6
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    Gene loops enhance transcriptional directionality (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-09-29
    Description: Eukaryotic genomes are extensively transcribed, forming both messenger RNAs (mRNAs) and noncoding RNAs (ncRNAs). ncRNAs made by RNA polymerase II often initiate from bidirectional promoters (nucleosome-depleted chromatin) that synthesize mRNA and ncRNA in opposite directions. We demonstrate that, by adopting a gene-loop conformation, actively transcribed mRNA encoding genes restrict divergent transcription of ncRNAs. Because gene-loop formation depends on a protein factor (Ssu72) that coassociates with both the promoter and the terminator, the inactivation of Ssu72 leads to increased synthesis of promoter-associated divergent ncRNAs, referred to as Ssu72-restricted transcripts (SRTs). Similarly, inactivation of individual gene loops by gene mutation enhances SRT synthesis. We demonstrate that gene-loop conformation enforces transcriptional directionality on otherwise bidirectional promoters.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3563069/" 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/PMC3563069/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tan-Wong, Sue Mei -- Zaugg, Judith B -- Camblong, Jurgi -- Xu, Zhenyu -- Zhang, David W -- Mischo, Hannah E -- Ansari, Aseem Z -- Luscombe, Nicholas M -- Steinmetz, Lars M -- Proudfoot, Nick J -- 091805/Wellcome Trust/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2012 Nov 2;338(6107):671-5. doi: 10.1126/science.1224350. Epub 2012 Sep 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford OX1 3RE, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23019609" target="_blank"〉PubMed〈/a〉
    Keywords: Exosome Multienzyme Ribonuclease Complex/metabolism ; *Genes, Fungal ; Genome, Fungal ; Mutation ; Nucleic Acid Conformation ; Phosphoprotein Phosphatases/metabolism ; Promoter Regions, Genetic ; RNA Polymerase II/metabolism ; RNA Stability ; RNA, Fungal/genetics/metabolism ; RNA, Messenger/*genetics/metabolism ; RNA, Untranslated/*genetics/metabolism ; Saccharomyces cerevisiae/*genetics/metabolism ; Saccharomyces cerevisiae Proteins/metabolism ; *Transcription, Genetic ; mRNA Cleavage and Polyadenylation Factors/metabolism
    Print ISSN: 0036-8075
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  • 7
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    Medicine. The ultimate genetic test (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Drmanac, Radoje -- New York, N.Y. -- Science. 2012 Jun 1;336(6085):1110-2. doi: 10.1126/science.1221037.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Complete Genomics, Inc., Mountain View, CA 94043, USA. rdrmanac@completegenomics.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22654043" target="_blank"〉PubMed〈/a〉
    Keywords: Genetic Predisposition to Disease ; Genetic Privacy ; *Genetic Testing/economics/methods/standards ; *Genetic Variation ; *Genome, Human ; Humans ; Mutation ; Precision Medicine ; Public Policy ; *Sequence Analysis, DNA/economics/methods/standards
    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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    Cancer research. Unraveling the obesity-cancer connection (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-01-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Taubes, Gary -- New York, N.Y. -- Science. 2012 Jan 6;335(6064):28, 30-2. doi: 10.1126/science.335.6064.28.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22223787" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Proliferation ; Diabetes Mellitus, Type 2/complications/*metabolism ; Diet ; Glucose/metabolism ; Humans ; Insulin/blood/*metabolism ; Mutation ; Neoplasms/*etiology/genetics/metabolism/pathology ; Obesity/complications/*metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Receptor, Insulin/metabolism ; Receptors, Somatomedin/metabolism ; Signal Transduction ; Somatomedins/*metabolism
    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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  • 9
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    IBI series winner. A mutant search--Caenorhabditis elegans and gene discovery (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-11-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉LaRue, Candace C -- Padilla, Pamela A -- New York, N.Y. -- Science. 2012 Oct 26;338(6106):487-8. doi: 10.1126/science.1215229.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, University of North Texas, Denton TX 76203, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23112325" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/*genetics ; Caenorhabditis elegans Proteins/*genetics ; DNA Mutational Analysis ; *Genetic Association Studies ; Genetic Research ; *Genetic Testing ; Genetics/*education ; Mutation ; Texas ; Universities
    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
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    The biology of genomes. Single-cell sequencing tackles basic and biomedical questions (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-05-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 2012 May 25;336(6084):976-7. doi: 10.1126/science.336.6084.976.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22628633" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/genetics ; Cell Line, Tumor ; Female ; Genes, Neoplasm ; *Genome, Human ; Humans ; Lab-On-A-Chip Devices ; Male ; Mutation ; Recombination, Genetic ; Sequence Analysis, DNA/*methods ; *Single-Cell Analysis ; Spermatozoa
    Print ISSN: 0036-8075
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  • 11
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    Sedlin controls the ER export of procollagen by regulating the Sar1 cycle (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-09-29
    Description: Newly synthesized proteins exit the endoplasmic reticulum (ER) via coat protein complex II (COPII) vesicles. Procollagen (PC), however, forms prefibrils that are too large to fit into typical COPII vesicles; PC thus needs large transport carriers, which we term megacarriers. TANGO1 assists PC packing, but its role in promoting the growth of megacarriers is not known. We found that TANGO1 recruited Sedlin, a TRAPP component that is defective in spondyloepiphyseal dysplasia tarda (SEDT), and that Sedlin was required for the ER export of PC. Sedlin bound and promoted efficient cycling of Sar1, a guanosine triphosphatase that can constrict membranes, and thus allowed nascent carriers to grow and incorporate PC prefibrils. This joint action of TANGO1 and Sedlin sustained the ER export of PC, and its derangement may explain the defective chondrogenesis underlying SEDT.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3471527/" 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/PMC3471527/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Venditti, Rossella -- Scanu, Tiziana -- Santoro, Michele -- Di Tullio, Giuseppe -- Spaar, Alexander -- Gaibisso, Renato -- Beznoussenko, Galina V -- Mironov, Alexander A -- Mironov, Alexander Jr -- Zelante, Leopoldo -- Piemontese, Maria Rosaria -- Notarangelo, Angelo -- Malhotra, Vivek -- Vertel, Barbara M -- Wilson, Cathal -- De Matteis, Maria Antonietta -- AR053696/AR/NIAMS NIH HHS/ -- GGP06166/Telethon/Italy -- GGP07075/Telethon/Italy -- GSP08002/Telethon/Italy -- GTF08001/Telethon/Italy -- New York, N.Y. -- Science. 2012 Sep 28;337(6102):1668-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Telethon Institute of Genetics and Medicine, Naples, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23019651" target="_blank"〉PubMed〈/a〉
    Keywords: Aryl Hydrocarbon Receptor Nuclear Translocator/*metabolism ; COP-Coated Vesicles/metabolism ; Cell Line ; Chondrogenesis/genetics ; Endoplasmic Reticulum/*metabolism ; Golgi Apparatus/metabolism ; Humans ; Membrane Transport Proteins/genetics/*metabolism ; Monomeric GTP-Binding Proteins/*metabolism ; Mutation ; Osteochondrodysplasias/genetics/metabolism ; Procollagen/*metabolism ; Protein Transport ; Transcription Factors/genetics/*metabolism
    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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  • 12
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    Pigment pattern formation by contact-dependent depolarization (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-02-11
    Description: Although recent experimental studies have suggested that the interactions among the pigment cells play a key role in the skin pattern formation, details of the mechanism remain largely unknown. By using an in vitro cell culture system, we have detected interactions between the two pigment cell types, melanophores and xanthophores, in the zebrafish skin. During primary culture, the melanophore membrane transiently depolarizes when contacted with the dendrites of a xanthophore. This depolarization triggers melanophore migration to avoid further contact with the xanthophores. Cell depolarization and repulsive movement were not observed in pigment cells with the jaguar mutant, which shows defective segregation of melanophores and xanthophores. The depolarization-repulsion of wild-type pigment cells may explain the pigment cell behaviors generating the stripe pattern of zebrafish.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Inaba, Masafumi -- Yamanaka, Hiroaki -- Kondo, Shigeru -- New York, N.Y. -- Science. 2012 Feb 10;335(6069):677. doi: 10.1126/science.1212821.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate School of Frontier Biosciences, Osaka University, 1-3 Yamadaoka, Suita, Osaka, 565-0871, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22323812" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Communication ; Cell Movement ; Cells, Cultured ; Chromatophores/*physiology ; Melanophores/*physiology ; Membrane Potentials ; Mutation ; Skin/cytology ; *Skin Pigmentation ; Zebrafish/*anatomy & histology/physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 13
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    An overlapping protein-coding region in influenza A virus segment 3 modulates the host response (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-30
    Description: Influenza A virus (IAV) infection leads to variable and imperfectly understood pathogenicity. We report that segment 3 of the virus contains a second open reading frame ("X-ORF"), accessed via ribosomal frameshifting. The frameshift product, termed PA-X, comprises the endonuclease domain of the viral PA protein with a C-terminal domain encoded by the X-ORF and functions to repress cellular gene expression. PA-X also modulates IAV virulence in a mouse infection model, acting to decrease pathogenicity. Loss of PA-X expression leads to changes in the kinetics of the global host response, which notably includes increases in inflammatory, apoptotic, and T lymphocyte-signaling pathways. Thus, we have identified a previously unknown IAV protein that modulates the host response to infection, a finding with important implications for understanding IAV pathogenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3552242/" 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/PMC3552242/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jagger, B W -- Wise, H M -- Kash, J C -- Walters, K-A -- Wills, N M -- Xiao, Y-L -- Dunfee, R L -- Schwartzman, L M -- Ozinsky, A -- Bell, G L -- Dalton, R M -- Lo, A -- Efstathiou, S -- Atkins, J F -- Firth, A E -- Taubenberger, J K -- Digard, P -- 073126/Wellcome Trust/United Kingdom -- 088789/Wellcome Trust/United Kingdom -- G0700815/Medical Research Council/United Kingdom -- G0700815(82260)/Medical Research Council/United Kingdom -- G9800943/Medical Research Council/United Kingdom -- MR/J002232/1/Medical Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2012 Jul 13;337(6091):199-204. doi: 10.1126/science.1222213. Epub 2012 Jun 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Virology, Department of Pathology, University of Cambridge, Cambridge CB2 1QP, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22745253" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; Codon ; Conserved Sequence ; Female ; *Frameshifting, Ribosomal ; Gene Expression Regulation ; Genome, Viral ; HEK293 Cells ; Humans ; Influenza A Virus, H1N1 Subtype/*genetics/growth & development/pathogenicity ; Influenza A virus/*genetics/metabolism ; Lung/pathology/virology ; Mice ; Mice, Inbred BALB C ; Molecular Sequence Data ; Mutation ; *Open Reading Frames ; Orthomyxoviridae Infections/genetics/immunology/pathology/*virology ; Protein Interaction Domains and Motifs ; Proteome ; RNA Replicase/chemistry/*genetics/*metabolism ; RNA, Messenger/genetics/metabolism ; RNA, Viral/genetics/metabolism ; Reassortant Viruses/genetics ; Repressor Proteins/chemistry/*genetics/*metabolism ; Viral Nonstructural Proteins/chemistry/*genetics/*metabolism ; Viral Proteins/biosynthesis/chemistry/*genetics/*metabolism ; Virus Replication
    Print ISSN: 0036-8075
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  • 14
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    Benefits and risks of influenza research: lessons learned (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-23
    Description: Given the yearly challenge of seasonal influenza and the potential catastrophic consequences of future pandemics, the need for intensive basic and clinical influenza research is unquestionable. Although the fruits of decades of research have enabled dramatic improvements in our ability to prevent and treat influenza, many fundamental questions remain, including those related to the complex factors associated with host switching and transmission of influenza viruses. Recent public concern over two H5N1 influenza manuscripts that studied the transmissibility of influenza viruses has triggered intense discussion on dual-use research and the way forward.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fauci, Anthony S -- Collins, Francis S -- New York, N.Y. -- Science. 2012 Jun 22;336(6088):1522-3. doi: 10.1126/science.1224305.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Institutes of Health, Bethesda, MD 20892, USA. afauci@niaid.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22723407" target="_blank"〉PubMed〈/a〉
    Keywords: Advisory Committees ; Animals ; *Biomedical Research ; Bioterrorism ; Disease Models, Animal ; Evolution, Molecular ; Ferrets ; Humans ; Influenza A Virus, H5N1 Subtype/*genetics/*pathogenicity ; Influenza, Human/mortality/transmission/*virology ; Mutation ; National Institutes of Health (U.S.) ; Orthomyxoviridae Infections/transmission/*virology ; Public Health ; Public Policy ; *Publishing ; Reassortant Viruses/genetics/pathogenicity ; Risk Assessment ; Security Measures ; United States
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  • 15
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    A core metabolic enzyme mediates resistance to phosphine gas (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-11-10
    Description: Phosphine is a small redox-active gas that is used to protect global grain reserves, which are threatened by the emergence of phosphine resistance in pest insects. We find that polymorphisms responsible for genetic resistance cluster around the redox-active catalytic disulfide or the dimerization interface of dihydrolipoamide dehydrogenase (DLD) in insects (Rhyzopertha dominica and Tribolium castaneum) and nematodes (Caenorhabditis elegans). DLD is a core metabolic enzyme representing a new class of resistance factor for a redox-active metabolic toxin. It participates in four key steps of core metabolism, and metabolite profiles indicate that phosphine exposure in mutant and wild-type animals affects these steps differently. Mutation of DLD in C. elegans increases arsenite sensitivity. This specific vulnerability may be exploited to control phosphine-resistant insects and safeguard food security.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schlipalius, David I -- Valmas, Nicholas -- Tuck, Andrew G -- Jagadeesan, Rajeswaran -- Ma, Li -- Kaur, Ramandeep -- Goldinger, Anita -- Anderson, Cameron -- Kuang, Jujiao -- Zuryn, Steven -- Mau, Yosep S -- Cheng, Qiang -- Collins, Patrick J -- Nayak, Manoj K -- Schirra, Horst Joachim -- Hilliard, Massimo A -- Ebert, Paul R -- R01NS060129/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2012 Nov 9;338(6108):807-10. doi: 10.1126/science.1224951.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Agri-Science Queensland, Department of Agriculture, Fisheries and Forestry, Ecosciences Precinct, Brisbane, QLD 4001, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23139334" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arsenicals/pharmacology ; Arsenites/pharmacology ; Beetles/drug effects/*enzymology/genetics/metabolism ; Caenorhabditis elegans/drug effects/*enzymology/genetics/metabolism ; Caenorhabditis elegans Proteins/chemistry/genetics/metabolism ; Catalytic Domain ; Dihydrolipoamide Dehydrogenase/chemistry/*genetics/metabolism ; Insect Proteins/chemistry/genetics/metabolism ; Insecticide Resistance/*genetics ; *Insecticides/pharmacology ; Metabolic Networks and Pathways ; Molecular Sequence Data ; Mutation ; Oxidation-Reduction ; Pesticides ; *Phosphines/pharmacology ; Polymorphism, Genetic ; Protein Multimerization ; Tribolium/drug effects/*enzymology/genetics/metabolism
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  • 16
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    Vitamin K2 is a mitochondrial electron carrier that rescues pink1 deficiency (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-05-15
    Description: Human UBIAD1 localizes to mitochondria and converts vitamin K(1) to vitamin K(2). Vitamin K(2) is best known as a cofactor in blood coagulation, but in bacteria it is a membrane-bound electron carrier. Whether vitamin K(2) exerts a similar carrier function in eukaryotic cells is unknown. We identified Drosophila UBIAD1/Heix as a modifier of pink1, a gene mutated in Parkinson's disease that affects mitochondrial function. We found that vitamin K(2) was necessary and sufficient to transfer electrons in Drosophila mitochondria. Heix mutants showed severe mitochondrial defects that were rescued by vitamin K(2), and, similar to ubiquinone, vitamin K(2) transferred electrons in Drosophila mitochondria, resulting in more efficient adenosine triphosphate (ATP) production. Thus, mitochondrial dysfunction was rescued by vitamin K(2) that serves as a mitochondrial electron carrier, helping to maintain normal ATP production.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vos, Melissa -- Esposito, Giovanni -- Edirisinghe, Janaka N -- Vilain, Sven -- Haddad, Dominik M -- Slabbaert, Jan R -- Van Meensel, Stefanie -- Schaap, Onno -- De Strooper, Bart -- Meganathan, R -- Morais, Vanessa A -- Verstreken, Patrik -- New York, N.Y. -- Science. 2012 Jun 8;336(6086):1306-10. doi: 10.1126/science.1218632. Epub 2012 May 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉VIB Center for the Biology of Disease, Leuven, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22582012" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Drosophila/genetics/*metabolism ; Drosophila Proteins/deficiency/*genetics/*metabolism ; *Electron Transport ; Escherichia coli/metabolism ; Flight, Animal ; Genes, Insect ; Membrane Potential, Mitochondrial ; Mitochondria/*metabolism/ultrastructure ; Mitochondria, Muscle/metabolism/ultrastructure ; Mutation ; Oxygen Consumption ; Protein-Serine-Threonine Kinases/deficiency/*genetics/*metabolism ; Ubiquinone/metabolism ; Ubiquitin-Protein Ligases/genetics ; Vitamin K 2/*metabolism/pharmacology
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  • 17
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    Structural biology. Versatility from protein disorder (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-09-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Babu, M Madan -- Kriwacki, Richard W -- Pappu, Rohit V -- MC_U105185859/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2012 Sep 21;337(6101):1460-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MRC Laboratory of Molecular Biology, Hills Road, Cambridge CB2 0QH, UK. madanm@mrc-lmb.cam.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22997313" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Computer Simulation ; Evolution, Molecular ; Mutation ; Protein Binding ; Protein Folding ; Protein Interaction Domains and Motifs ; Protein Structure, Tertiary ; Proteins/*chemistry/genetics/*metabolism
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  • 18
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    Avian influenza. For young scientists, a wild ride (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Enserink, Martin -- New York, N.Y. -- Science. 2012 Jun 22;336(6088):1495. doi: 10.1126/science.336.6088.1495.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22723388" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cough ; Ferrets ; *Influenza A Virus, H5N1 Subtype/genetics/pathogenicity ; Mutation ; Orthomyxoviridae Infections/transmission/*virology ; Publishing ; *Research Personnel ; Sneezing
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  • 19
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    Personalized medicine. New cystic fibrosis drug offers hope, at a price (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-02-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, Jocelyn -- New York, N.Y. -- Science. 2012 Feb 10;335(6069):645. doi: 10.1126/science.335.6069.645.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22323790" target="_blank"〉PubMed〈/a〉
    Keywords: Aminophenols/economics/*therapeutic use ; Cystic Fibrosis/*drug therapy/*genetics ; Cystic Fibrosis Transmembrane Conductance ; Regulator/chemistry/*genetics/metabolism ; Drug Approval ; Drug Costs ; Humans ; Molecular Targeted Therapy ; Mutation ; Precision Medicine ; Quinolones/economics/*therapeutic use ; Small Molecule Libraries ; United States ; United States Food and Drug Administration
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  • 20
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    The amyloid precursor protein has a flexible transmembrane domain and binds cholesterol (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-06-02
    Description: C99 is the transmembrane carboxyl-terminal domain of the amyloid precursor protein that is cleaved by gamma-secretase to release the amyloid-beta polypeptides, which are associated with Alzheimer's disease. Nuclear magnetic resonance and electron paramagnetic resonance spectroscopy show that the extracellular amino terminus of C99 includes a surface-embedded "N-helix" followed by a short "N-loop" connecting to the transmembrane domain (TMD). The TMD is a flexibly curved alpha helix, making it well suited for processive cleavage by gamma-secretase. Titration of C99 reveals a binding site for cholesterol, providing mechanistic insight into how cholesterol promotes amyloidogenesis. Membrane-buried GXXXG motifs (G, Gly; X, any amino acid), which have an established role in oligomerization, were also shown to play a key role in cholesterol binding. The structure and cholesterol binding properties of C99 may aid in the design of Alzheimer's therapeutics.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3528355/" 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/PMC3528355/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barrett, Paul J -- Song, Yuanli -- Van Horn, Wade D -- Hustedt, Eric J -- Schafer, Johanna M -- Hadziselimovic, Arina -- Beel, Andrew J -- Sanders, Charles R -- F31 NS077681/NS/NINDS NIH HHS/ -- P01 GM080513/GM/NIGMS NIH HHS/ -- T32 GM008320/GM/NIGMS NIH HHS/ -- T32 GM08320/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2012 Jun 1;336(6085):1168-71. doi: 10.1126/science.1219988.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Center for Structural Biology and Institute of Chemical Biology, Vanderbilt University School of Medicine, Nashville, TN 37232 USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22654059" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Amino Acid Sequence ; Amyloid beta-Protein Precursor/*chemistry/genetics/*metabolism ; Binding Sites ; Cholesterol/*metabolism ; Electron Spin Resonance Spectroscopy ; Humans ; Micelles ; Molecular Sequence Data ; Mutation ; Nuclear Magnetic Resonance, Biomolecular ; Peptide Fragments/*chemistry/genetics/*metabolism ; Protein Binding ; Protein Structure, Secondary ; Protein Structure, Tertiary
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  • 21
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    The transcription factor c-Maf controls touch receptor development and function (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-02-22
    Description: The sense of touch relies on detection of mechanical stimuli by specialized mechanosensory neurons. The scarcity of molecular data has made it difficult to analyze development of mechanoreceptors and to define the basis of their diversity and function. We show that the transcription factor c-Maf/c-MAF is crucial for mechanosensory function in mice and humans. The development and function of several rapidly adapting mechanoreceptor types are disrupted in c-Maf mutant mice. In particular, Pacinian corpuscles, a type of mechanoreceptor specialized to detect high-frequency vibrations, are severely atrophied. In line with this, sensitivity to high-frequency vibration is reduced in humans carrying a dominant mutation in the c-MAF gene. Thus, our work identifies a key transcription factor specifying development and function of mechanoreceptors and their end organs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wende, Hagen -- Lechner, Stefan G -- Cheret, Cyril -- Bourane, Steeve -- Kolanczyk, Maria E -- Pattyn, Alexandre -- Reuter, Katja -- Munier, Francis L -- Carroll, Patrick -- Lewin, Gary R -- Birchmeier, Carmen -- New York, N.Y. -- Science. 2012 Mar 16;335(6074):1373-6. doi: 10.1126/science.1214314. Epub 2012 Feb 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Developmental Biology, Max Delbruck Center (MDC) for Molecular Medicine, Berlin, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22345400" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ganglia, Spinal/cytology/embryology ; Gene Expression Regulation, Developmental ; Humans ; Maf Transcription Factors, Large/genetics/metabolism ; Mechanoreceptors/*cytology/*physiology ; Mice ; Mutation ; Pacinian Corpuscles/cytology/physiology ; Proto-Oncogene Proteins c-maf/genetics/*metabolism ; Proto-Oncogene Proteins c-ret/genetics/metabolism ; Skin/innervation ; *Touch ; Vibration
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  • 22
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    Assembly of an evolutionarily new pathway for alpha-pyrone biosynthesis in Arabidopsis (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-08-28
    Description: Plants possess arrays of functionally diverse specialized metabolites, many of which are distributed taxonomically. Here, we describe the evolution of a class of substituted alpha-pyrone metabolites in Arabidopsis, which we have named arabidopyrones. The biosynthesis of arabidopyrones requires a cytochrome P450 enzyme (CYP84A4) to generate the catechol-substituted substrate for an extradiol ring-cleavage dioxygenase (AtLigB). Unlike other ring-cleavage-derived plant metabolites made from tyrosine, arabidopyrones are instead derived from phenylalanine through the early steps of phenylpropanoid metabolism. Whereas CYP84A4, an Arabidopsis-specific paralog of the lignin-biosynthetic enzyme CYP84A1, has neofunctionalized relative to its ancestor, AtLigB homologs are widespread among land plants and many bacteria. This study exemplifies the rapid evolution of a biochemical pathway formed by the addition of a new biological activity into an existing metabolic infrastructure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weng, Jing-Ke -- Li, Yi -- Mo, Huaping -- Chapple, Clint -- New York, N.Y. -- Science. 2012 Aug 24;337(6097):960-4. doi: 10.1126/science.1221614.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Purdue University, West Lafayette, IN 47907, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22923580" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Arabidopsis/enzymology/genetics/*metabolism ; Arabidopsis Proteins/chemistry/genetics/*metabolism ; Base Sequence ; Biosynthetic Pathways ; Catalytic Domain ; Cytochrome P-450 Enzyme System/chemistry/genetics/*metabolism ; Dioxygenases/genetics/metabolism ; Evolution, Molecular ; Gene Duplication ; Genome, Plant ; Models, Molecular ; Molecular Sequence Data ; Mutation ; Phenylalanine/metabolism ; Phylogeny ; Plant Stems/metabolism ; Plants, Genetically Modified ; Pyrones/chemistry/*metabolism
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    Tricking the guard: exploiting plant defense for disease susceptibility (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-10-23
    Description: Typically, pathogens deploy virulence effectors to disable defense. Plants defeat effectors with resistance proteins that guard effector targets. We found that a pathogen exploits a resistance protein by activating it to confer susceptibility in Arabidopsis. The guard mechanism of plant defense is recapitulated by interactions among victorin (an effector produced by the necrotrophic fungus Cochliobolus victoriae), TRX-h5 (a defense-associated thioredoxin), and LOV1 (an Arabidopsis susceptibility protein). In LOV1's absence, victorin inhibits TRX-h5, resulting in compromised defense but not disease by C. victoriae. In LOV1's presence, victorin binding to TRX-h5 activates LOV1 and elicits a resistance-like response that confers disease susceptibility. We propose that victorin is, or mimics, a conventional pathogen virulence effector that was defeated by LOV1 and confers virulence to C. victoriae solely because it incites defense.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4125361/" 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/PMC4125361/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lorang, J -- Kidarsa, T -- Bradford, C S -- Gilbert, B -- Curtis, M -- Tzeng, S-C -- Maier, C S -- Wolpert, T J -- BB/D016541/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/H008039/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- P30 ES000210/ES/NIEHS NIH HHS/ -- P30ES200210/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 2012 Nov 2;338(6107):659-62. doi: 10.1126/science.1226743. Epub 2012 Oct 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Botany and Plant Pathology and Center for Genome Research and Biocomputing, Oregon State University, Corvallis, OR 97331, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23087001" target="_blank"〉PubMed〈/a〉
    Keywords: *Arabidopsis/immunology/metabolism/microbiology ; Arabidopsis Proteins/chemistry/genetics/*metabolism ; Ascomycota/metabolism/*pathogenicity ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Disease Susceptibility ; Fungal Proteins/*metabolism ; Mutation ; Mycotoxins/*metabolism ; Oxidation-Reduction ; *Plant Diseases/immunology/microbiology ; *Plant Immunity ; Protein Binding ; Protein Interaction Domains and Motifs ; Thioredoxins/genetics/*metabolism ; Tobacco/genetics/metabolism ; Virulence Factors/*metabolism
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    Population genomics of early events in the ecological differentiation of bacteria (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-04-12
    Description: Genetic exchange is common among bacteria, but its effect on population diversity during ecological differentiation remains controversial. A fundamental question is whether advantageous mutations lead to selection of clonal genomes or, as in sexual eukaryotes, sweep through populations on their own. Here, we show that in two recently diverged populations of ocean bacteria, ecological differentiation has occurred akin to a sexual mechanism: A few genome regions have swept through subpopulations in a habitat-specific manner, accompanied by gradual separation of gene pools as evidenced by increased habitat specificity of the most recent recombinations. These findings reconcile previous, seemingly contradictory empirical observations of the genetic structure of bacterial populations and point to a more unified process of differentiation in bacteria and sexual eukaryotes than previously thought.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3337212/" 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/PMC3337212/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shapiro, B Jesse -- Friedman, Jonathan -- Cordero, Otto X -- Preheim, Sarah P -- Timberlake, Sonia C -- Szabo, Gitta -- Polz, Martin F -- Alm, Eric J -- U54 GM088558/GM/NIGMS NIH HHS/ -- U54 GM088558-02/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2012 Apr 6;336(6077):48-51. doi: 10.1126/science.1218198.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Computational and Systems Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22491847" target="_blank"〉PubMed〈/a〉
    Keywords: Chromosomes, Bacterial/genetics ; *Ecosystem ; *Evolution, Molecular ; Gene Flow ; Gene Transfer, Horizontal ; Genes, Bacterial ; Genetic Variation ; *Genome, Bacterial ; Models, Genetic ; Molecular Sequence Data ; Mutation ; Oceans and Seas ; Phylogeny ; Polymorphism, Single Nucleotide ; *Recombination, Genetic ; Seawater/*microbiology ; *Selection, Genetic ; Vibrio/classification/*genetics
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    Neuroscience. All eyes on RNA (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-12-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Garber, Ken -- New York, N.Y. -- Science. 2012 Dec 7;338(6112):1282-3. doi: 10.1126/science.338.6112.1282.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23224536" target="_blank"〉PubMed〈/a〉
    Keywords: Amyotrophic Lateral Sclerosis/*genetics/metabolism ; Chromosomes, Human, Pair 9/genetics ; DNA-Binding Proteins/genetics/metabolism ; Dementia/genetics/metabolism ; Humans ; Motor Neurons/metabolism/pathology ; Mutation ; Proteins/genetics ; RNA/*metabolism ; RNA-Binding Protein FUS/genetics/metabolism ; RNA-Binding Proteins/*genetics/metabolism
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    Cytoplasmic ATP hydrolysis powers transport of lipopolysaccharide across the periplasm in E. coli (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-11-10
    Description: Millions of molecules of lipopolysaccharide (LPS) must be assembled on the Escherichia coli cell surface each time the cell divides. The biogenesis of LPS requires seven essential lipopolysaccharide transport (Lpt) proteins to move LPS from the inner membrane through the periplasm to the cell surface. However, no intermediate transport states have been observed. We developed methods to observe intermediate LPS molecules bound to Lpt proteins in the process of being transported in vivo. Movement of individual LPS molecules along these binding sites required multiple rounds of adenosine triphosphate (ATP) hydrolysis in vitro, which suggests that ATP is used to push a continuous stream of LPS through a transenvelope bridge in discrete steps against a concentration gradient.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3552488/" 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/PMC3552488/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Okuda, Suguru -- Freinkman, Elizaveta -- Kahne, Daniel -- AI081059/AI/NIAID NIH HHS/ -- GM066174/GM/NIGMS NIH HHS/ -- R01 AI081059/AI/NIAID NIH HHS/ -- R01 GM066174/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2012 Nov 30;338(6111):1214-7. doi: 10.1126/science.1228984. Epub 2012 Nov 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Chemical Biology, Harvard University, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23138981" target="_blank"〉PubMed〈/a〉
    Keywords: ATP-Binding Cassette Transporters/chemistry/metabolism ; Adenosine Triphosphate/*metabolism ; Bacterial Proteins/chemistry/metabolism ; Biological Transport ; Carrier Proteins/chemistry/genetics/metabolism ; Cytoplasm/*metabolism ; Escherichia coli/*metabolism ; Escherichia coli Proteins/chemistry/genetics/metabolism ; Hydrolysis ; Lipopolysaccharides/*metabolism ; Membrane Proteins/chemistry/genetics/metabolism ; Mutation ; Periplasm/*metabolism ; Protein Conformation
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    Glacial survival of boreal trees in northern Scandinavia (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-03
    Description: It is commonly believed that trees were absent in Scandinavia during the last glaciation and first recolonized the Scandinavian Peninsula with the retreat of its ice sheet some 9000 years ago. Here, we show the presence of a rare mitochondrial DNA haplotype of spruce that appears unique to Scandinavia and with its highest frequency to the west-an area believed to sustain ice-free refugia during most of the last ice age. We further show the survival of DNA from this haplotype in lake sediments and pollen of Trondelag in central Norway dating back ~10,300 years and chloroplast DNA of pine and spruce in lake sediments adjacent to the ice-free Andoya refugium in northwestern Norway as early as ~22,000 and 17,700 years ago, respectively. Our findings imply that conifer trees survived in ice-free refugia of Scandinavia during the last glaciation, challenging current views on survival and spread of trees as a response to climate changes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Parducci, Laura -- Jorgensen, Tina -- Tollefsrud, Mari Mette -- Elverland, Ellen -- Alm, Torbjorn -- Fontana, Sonia L -- Bennett, K D -- Haile, James -- Matetovici, Irina -- Suyama, Yoshihisa -- Edwards, Mary E -- Andersen, Kenneth -- Rasmussen, Morten -- Boessenkool, Sanne -- Coissac, Eric -- Brochmann, Christian -- Taberlet, Pierre -- Houmark-Nielsen, Michael -- Larsen, Nicolaj Krog -- Orlando, Ludovic -- Gilbert, M Thomas P -- Kjaer, Kurt H -- Alsos, Inger Greve -- Willerslev, Eske -- New York, N.Y. -- Science. 2012 Mar 2;335(6072):1083-6. doi: 10.1126/science.1216043.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ecology and Genetics, Evolutionary Biology Centre, Uppsala University, Uppsala, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22383845" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; DNA, Chloroplast/genetics ; DNA, Mitochondrial/genetics ; *Ecosystem ; Europe ; *Fossils ; Geologic Sediments ; Haplotypes ; *Ice Cover ; Molecular Sequence Data ; Mutation ; Norway ; *Picea/genetics ; *Pinus/genetics ; Scandinavian and Nordic Countries ; Time
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    Cell biology. The unusual case of Porcupine (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-08-28
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4314091/" 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/PMC4314091/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lum, Lawrence -- Clevers, Hans -- R21 HD061303/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2012 Aug 24;337(6097):922-3. doi: 10.1126/science.1228179.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390, USA. lawrence.lum@utsouthwestern.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22923569" target="_blank"〉PubMed〈/a〉
    Keywords: Antineoplastic Agents/pharmacology/*therapeutic use ; Clinical Trials, Phase I as Topic ; DNA-Binding Proteins/genetics ; Drug Discovery ; Enzyme Inhibitors/pharmacology/*therapeutic use ; Humans ; Membrane Proteins/*antagonists & inhibitors/genetics/*metabolism ; Molecular Targeted Therapy ; Mutation ; Neoplasms/*drug therapy/genetics/metabolism ; Oncogene Proteins/genetics ; Palmitic Acid/metabolism ; Protein-Serine-Threonine Kinases/genetics ; Wnt Proteins/*metabolism ; Wnt Signaling Pathway/*drug effects
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    IBI* series winner. Adapting to osmotic stress and the process of science (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gasper, Brittany J -- Minchella, Dennis J -- Weaver, Gabriela C -- Csonka, Laszlo N -- Gardner, Stephanie M -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Mar 30;335(6076):1590-1. doi: 10.1126/science.1215582.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Purdue University, West Lafayette, IN 47907, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22461603" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptation, Physiological ; Awards and Prizes ; Bacterial Proteins/genetics/metabolism ; Genetics, Microbial/*education ; Mutation ; Osmotic Pressure ; Research/*education ; Salmonella typhimurium/*genetics/physiology ; *Stress, Physiological ; Symporters/genetics/metabolism ; Universities
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    dSarm/Sarm1 is required for activation of an injury-induced axon death pathway (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-09
    Description: Axonal and synaptic degeneration is a hallmark of peripheral neuropathy, brain injury, and neurodegenerative disease. Axonal degeneration has been proposed to be mediated by an active autodestruction program, akin to apoptotic cell death; however, loss-of-function mutations capable of potently blocking axon self-destruction have not been described. Here, we show that loss of the Drosophila Toll receptor adaptor dSarm (sterile alpha/Armadillo/Toll-Interleukin receptor homology domain protein) cell-autonomously suppresses Wallerian degeneration for weeks after axotomy. Severed mouse Sarm1 null axons exhibit remarkable long-term survival both in vivo and in vitro, indicating that Sarm1 prodegenerative signaling is conserved in mammals. Our results provide direct evidence that axons actively promote their own destruction after injury and identify dSarm/Sarm1 as a member of an ancient axon death signaling pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Osterloh, Jeannette M -- Yang, Jing -- Rooney, Timothy M -- Fox, A Nicole -- Adalbert, Robert -- Powell, Eric H -- Sheehan, Amy E -- Avery, Michelle A -- Hackett, Rachel -- Logan, Mary A -- MacDonald, Jennifer M -- Ziegenfuss, Jennifer S -- Milde, Stefan -- Hou, Ying-Ju -- Nathan, Carl -- Ding, Aihao -- Brown, Robert H Jr -- Conforti, Laura -- Coleman, Michael -- Tessier-Lavigne, Marc -- Zuchner, Stephan -- Freeman, Marc R -- 5R01-NS050557-05/NS/NINDS NIH HHS/ -- AI030165/AI/NIAID NIH HHS/ -- R01NS059991/NS/NINDS NIH HHS/ -- R01NS072248/NS/NINDS NIH HHS/ -- RC2-NS070-342/NS/NINDS NIH HHS/ -- U54NS065712/NS/NINDS NIH HHS/ -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Jul 27;337(6093):481-4. doi: 10.1126/science.1223899. Epub 2012 Jun 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, University of Massachusetts Medical School, Worcester, MA 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22678360" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Apoptosis ; Armadillo Domain Proteins/analysis/*genetics/*physiology ; Axons/*physiology/ultrastructure ; Axotomy ; Cell Survival ; Cells, Cultured ; Cytoskeletal Proteins/analysis/*genetics/*physiology ; Denervation ; Drosophila/embryology/genetics/physiology ; Drosophila Proteins/analysis/*genetics/*physiology ; Mice ; Mutation ; Neurons/*physiology ; Sciatic Nerve/injuries/physiology ; Signal Transduction ; Superior Cervical Ganglion/cytology ; Tissue Culture Techniques ; *Wallerian Degeneration
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    Recent explosive human population growth has resulted in an excess of rare genetic variants (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-05-15
    Description: Human populations have experienced recent explosive growth, expanding by at least three orders of magnitude over the past 400 generations. This departure from equilibrium skews patterns of genetic variation and distorts basic principles of population genetics. We characterized the empirical signatures of explosive growth on the site frequency spectrum and found that the discrepancy in rare variant abundance across demographic modeling studies is mostly due to differences in sample size. Rapid recent growth increases the load of rare variants and is likely to play a role in the individual genetic burden of complex disease risk. Hence, the extreme recent human population growth needs to be taken into consideration in studying the genetics of complex diseases and traits.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3586590/" 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/PMC3586590/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Keinan, Alon -- Clark, Andrew G -- GM065509/GM/NIGMS NIH HHS/ -- HL102419/HL/NHLBI NIH HHS/ -- R01 HG003229/HG/NHGRI NIH HHS/ -- RC2 HL102419/HL/NHLBI NIH HHS/ -- U01 HG005715/HG/NHGRI NIH HHS/ -- U01-HG005715/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2012 May 11;336(6082):740-3. doi: 10.1126/science.1217283.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Statistics and Computational Biology, Cornell University, Ithaca, NY 14853, USA. ak735@cornell.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22582263" target="_blank"〉PubMed〈/a〉
    Keywords: Asian Continental Ancestry Group/genetics ; European Continental Ancestry Group/genetics ; Gene Frequency ; Genetic Association Studies ; Genetic Predisposition to Disease ; *Genetic Variation ; Genetics, Population/methods ; Genome, Human ; Haplotypes ; Heterozygote ; Humans ; Models, Genetic ; Mutation ; Polymorphism, Single Nucleotide ; *Population Density ; *Population Growth ; Sample Size ; Sequence Analysis, DNA
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    The structure and catalytic cycle of a sodium-pumping pyrophosphatase (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-07-28
    Description: Membrane-integral pyrophosphatases (M-PPases) are crucial for the survival of plants, bacteria, and protozoan parasites. They couple pyrophosphate hydrolysis or synthesis to Na(+) or H(+) pumping. The 2.6-angstrom structure of Thermotoga maritima M-PPase in the resting state reveals a previously unknown solution for ion pumping. The hydrolytic center, 20 angstroms above the membrane, is coupled to the gate formed by the conserved Asp(243), Glu(246), and Lys(707) by an unusual "coupling funnel" of six alpha helices. Comparison with our 4.0-angstrom resolution structure of the product complex suggests that helix 12 slides down upon substrate binding to open the gate by a simple binding-change mechanism. Below the gate, four helices form the exit channel. Superimposing helices 3 to 6, 9 to 12, and 13 to 16 suggests that M-PPases arose through gene triplication.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kellosalo, Juho -- Kajander, Tommi -- Kogan, Konstantin -- Pokharel, Kisun -- Goldman, Adrian -- New York, N.Y. -- Science. 2012 Jul 27;337(6093):473-6. doi: 10.1126/science.1222505.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Structural Biology and Biophysics Program, Institute of Biotechnology, Post Office Box 65, University of Helsinki, FIN-00014, Finland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22837527" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Bacterial Proteins/chemistry/genetics/metabolism ; Biocatalysis ; Calcium/chemistry ; Catalytic Domain ; Cell Membrane/enzymology ; Crystallography, X-Ray ; Diphosphates/*metabolism ; Hydrolysis ; Hydrophobic and Hydrophilic Interactions ; Ion Channel Gating ; Magnesium/chemistry ; Models, Molecular ; Molecular Sequence Data ; Mutation ; Protein Conformation ; Protein Multimerization ; Protein Structure, Secondary ; Pyrophosphatases/*chemistry/genetics/*metabolism ; Sodium/*metabolism ; Sodium-Potassium-Exchanging ATPase/*chemistry/genetics/metabolism ; Thermotoga maritima/*enzymology
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    Natural variation in a chloride channel subunit confers avermectin resistance in C. elegans (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-02-04
    Description: Resistance of nematodes to anthelmintics such as avermectins has emerged as a major global health and agricultural problem, but genes conferring natural resistance to avermectins are unknown. We show that a naturally occurring four-amino-acid deletion in the ligand-binding domain of GLC-1, the alpha-subunit of a glutamate-gated chloride channel, confers resistance to avermectins in the model nematode Caenorhabditis elegans. We also find that the same variant confers resistance to the avermectin-producing bacterium Streptomyces avermitilis. Population-genetic analyses identified two highly divergent haplotypes at the glc-1 locus that have been maintained at intermediate frequencies by long-term balancing selection. These results implicate variation in glutamate-gated chloride channels in avermectin resistance and provide a mechanism by which such resistance can be maintained.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3273849/" 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/PMC3273849/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ghosh, Rajarshi -- Andersen, Erik C -- Shapiro, Joshua A -- Gerke, Justin P -- Kruglyak, Leonid -- P50-GM071508/GM/NIGMS NIH HHS/ -- R01 HG004321/HG/NHGRI NIH HHS/ -- R01 HG004321-03/HG/NHGRI NIH HHS/ -- R01-HG004321/HG/NHGRI NIH HHS/ -- R37- MH59520/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Feb 3;335(6068):574-8. doi: 10.1126/science.1214318.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lewis-Sigler Institute for Integrative Genomics, Department of Ecology and Evolutionary Biology, and Howard Hughes Medical Institute, Princeton University, Princeton, NJ 08544, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22301316" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Animals, Genetically Modified ; Antinematodal Agents/*pharmacology ; Caenorhabditis elegans/*drug effects/*genetics/physiology ; Caenorhabditis elegans Proteins/chemistry/*genetics/metabolism ; Chloride Channels/chemistry/*genetics/metabolism ; Crosses, Genetic ; Drug Resistance/genetics ; Genes, Helminth ; Genome-Wide Association Study ; Ivermectin/*analogs & derivatives/*pharmacology ; Ligands ; Molecular Sequence Data ; Mutation ; Polymorphism, Single Nucleotide ; Protein Structure, Tertiary ; Quantitative Trait Loci ; Selection, Genetic ; Streptomyces/physiology
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    ER cargo properties specify a requirement for COPII coat rigidity mediated by Sec13p (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-02-04
    Description: Eukaryotic secretory proteins exit the endoplasmic reticulum (ER) via transport vesicles generated by the essential coat protein complex II (COPII) proteins. The outer coat complex, Sec13-Sec31, forms a scaffold that is thought to enforce curvature. By exploiting yeast bypass-of-sec-thirteen (bst) mutants, where Sec13p is dispensable, we probed the relationship between a compromised COPII coat and the cellular context in which it could still function. Genetic and biochemical analyses suggested that Sec13p was required to generate vesicles from membranes that contained asymmetrically distributed cargoes that were likely to confer opposing curvature. Thus, Sec13p may rigidify the COPII cage and increase its membrane-bending capacity; this function could be bypassed when a bst mutation renders the membrane more deformable.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3306526/" 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/PMC3306526/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Copic, Alenka -- Latham, Catherine F -- Horlbeck, Max A -- D'Arcangelo, Jennifer G -- Miller, Elizabeth A -- GM078186/GM/NIGMS NIH HHS/ -- GM085089/GM/NIGMS NIH HHS/ -- R01 GM078186/GM/NIGMS NIH HHS/ -- R01 GM078186-05/GM/NIGMS NIH HHS/ -- R01 GM085089/GM/NIGMS NIH HHS/ -- R01 GM085089-04/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2012 Mar 16;335(6074):1359-62. doi: 10.1126/science.1215909. Epub 2012 Feb 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Columbia University, New York, NY 10027, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22300850" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; COP-Coated Vesicles/*chemistry/metabolism/ultrastructure ; Endoplasmic Reticulum/*metabolism ; Genes, Fungal ; Models, Biological ; Models, Molecular ; Mutant Proteins/chemistry/metabolism ; Mutation ; Nuclear Pore Complex Proteins/chemistry/genetics/*metabolism ; Protein Interaction Domains and Motifs ; Protein Structure, Tertiary ; Protein Transport ; Saccharomyces cerevisiae/genetics/*metabolism/ultrastructure ; Saccharomyces cerevisiae Proteins/chemistry/genetics/*metabolism ; Vesicular Transport Proteins/chemistry/metabolism
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    Mitochondrial fission, fusion, and stress (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-09-01
    Description: Mitochondrial fission and fusion play critical roles in maintaining functional mitochondria when cells experience metabolic or environmental stresses. Fusion helps mitigate stress by mixing the contents of partially damaged mitochondria as a form of complementation. Fission is needed to create new mitochondria, but it also contributes to quality control by enabling the removal of damaged mitochondria and can facilitate apoptosis during high levels of cellular stress. Disruptions in these processes affect normal development, and they have been implicated in neurodegenerative diseases, such as Parkinson's.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4762028/" 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/PMC4762028/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Youle, Richard J -- van der Bliek, Alexander M -- GM051866/GM/NIGMS NIH HHS/ -- Z99 NS999999/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2012 Aug 31;337(6098):1062-5. doi: 10.1126/science.1219855.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA. youler@ninds.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22936770" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autophagy ; DNA, Mitochondrial/genetics ; Humans ; *Membrane Fusion ; Mice ; Mitochondria/genetics/*physiology ; Mitochondrial Diseases/metabolism ; Mitochondrial Proteins/genetics/metabolism ; Mutation ; Neurodegenerative Diseases/metabolism ; Parkinson Disease/metabolism ; *Stress, Physiological
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    Neuroscience. The emerging biology of autism spectrum disorders (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-09-18
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3657753/" 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/PMC3657753/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉State, Matthew W -- Sestan, Nenad -- P50MH081756/MH/NIMH NIH HHS/ -- R01 NS054273/NS/NINDS NIH HHS/ -- R01MH081754/MH/NIMH NIH HHS/ -- R01NS054273/NS/NINDS NIH HHS/ -- RC2MH089956/MH/NIMH NIH HHS/ -- U01 MH081896/MH/NIMH NIH HHS/ -- U01MH081896/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2012 Sep 14;337(6100):1301-3. doi: 10.1126/science.1224989.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Child Study Center and Department of Psychiatry, Yale University School of Medicine, New Haven, CT 06510, USA. matthew.state@yale.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22984058" target="_blank"〉PubMed〈/a〉
    Keywords: Child Development Disorders, Pervasive/*genetics ; Child, Preschool ; Gene Expression Profiling ; *Gene Expression Regulation, Developmental ; Genetic Loci ; Humans ; Mutation ; Neocortex/*growth & development/metabolism
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    A mutation in EGF repeat-8 of Notch discriminates between Serrate/Jagged and Delta family ligands (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-12-01
    Description: Notch signaling affects many developmental and cellular processes and has been implicated in congenital disorders, stroke, and numerous cancers. The Notch receptor binds its ligands Delta and Serrate and is able to discriminate between them in different contexts. However, the specific domains in Notch responsible for this selectivity are poorly defined. Through genetic screens in Drosophila, we isolated a mutation, Notch(jigsaw), that affects Serrate- but not Delta-dependent signaling. Notch(jigsaw) carries a missense mutation in epidermal growth factor repeat-8 (EGFr-8) and is defective in Serrate binding. A homologous point mutation in mammalian Notch2 also exhibits defects in signaling of a mammalian Serrate homolog, Jagged1. Hence, an evolutionarily conserved valine in EGFr-8 is essential for ligand selectivity and provides a molecular handle to study numerous Notch-dependent signaling events.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3663443/" 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/PMC3663443/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yamamoto, Shinya -- Charng, Wu-Lin -- Rana, Nadia A -- Kakuda, Shinako -- Jaiswal, Manish -- Bayat, Vafa -- Xiong, Bo -- Zhang, Ke -- Sandoval, Hector -- David, Gabriela -- Wang, Hao -- Haltiwanger, Robert S -- Bellen, Hugo J -- 1RC4GM096355-01/GM/NIGMS NIH HHS/ -- 5K12GM084897/GM/NIGMS NIH HHS/ -- 5P30HD024064/HD/NICHD NIH HHS/ -- 5R01GM061126-12/GM/NIGMS NIH HHS/ -- 5R01GM067858/GM/NIGMS NIH HHS/ -- 5T32-HD055200/HD/NICHD NIH HHS/ -- K12 GM084897/GM/NIGMS NIH HHS/ -- P30 HD024064/HD/NICHD NIH HHS/ -- R01 GM061126/GM/NIGMS NIH HHS/ -- R01 GM067858/GM/NIGMS NIH HHS/ -- RC4 GM096355/GM/NIGMS NIH HHS/ -- T32 HD055200/HD/NICHD NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Nov 30;338(6111):1229-32. doi: 10.1126/science.1228745.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Developmental Biology, Baylor College of Medicine, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23197537" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Calcium-Binding Proteins/*metabolism ; Cells, Cultured ; DNA Mutational Analysis ; Drosophila Proteins/*genetics/*metabolism ; Drosophila melanogaster/genetics/*metabolism ; Epidermal Growth Factor/genetics ; Evolution, Molecular ; Humans ; Intercellular Signaling Peptides and Proteins/*metabolism ; Intracellular Signaling Peptides and Proteins/*metabolism ; Ligands ; Male ; Membrane Proteins/*metabolism ; Methionine/genetics ; Molecular Sequence Data ; Mutation ; Receptor, Notch2/genetics/metabolism ; Receptors, Notch/*genetics/*metabolism ; Tandem Repeat Sequences/genetics ; Valine/genetics ; X Chromosome/genetics
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    Bacterial quorum sensing and metabolic incentives to cooperate (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-10-16
    Description: The opportunistic pathogen Pseudomonas aeruginosa uses a cell-cell communication system termed "quorum sensing" to control production of public goods, extracellular products that can be used by any community member. Not all individuals respond to quorum-sensing signals and synthesize public goods. Such social cheaters enjoy the benefits of the products secreted by cooperators. There are some P. aeruginosa cellular enzymes controlled by quorum sensing, and we show that quorum sensing-controlled expression of such private goods can put a metabolic constraint on social cheating and prevent a tragedy of the commons. Metabolic constraint of social cheating provides an explanation for private-goods regulation by a cooperative system and has general implications for population biology, infection control, and stabilization of quorum-sensing circuits in synthetic biology.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3587168/" 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/PMC3587168/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dandekar, Ajai A -- Chugani, Sudha -- Greenberg, E Peter -- GM-59026/GM/NIGMS NIH HHS/ -- P30 DK 89507/DK/NIDDK NIH HHS/ -- P30 DK089507/DK/NIDDK NIH HHS/ -- R01 GM059026/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2012 Oct 12;338(6104):264-6. doi: 10.1126/science.1227289.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Pulmonary and Critical Care Medicine, University of Washington School of Medicine, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23066081" target="_blank"〉PubMed〈/a〉
    Keywords: Acyl-Butyrolactones/metabolism ; Adenosine/*metabolism ; Bacterial Proteins/genetics/metabolism ; Caseins/metabolism ; Culture Media/metabolism ; Microarray Analysis ; Mutation ; Pseudomonas aeruginosa/genetics/*growth & development/*metabolism ; Quorum Sensing/genetics/*physiology ; Signal Transduction ; Social Behavior ; Trans-Activators/genetics/metabolism
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    Sex-specific adaptation drives early sex chromosome evolution in Drosophila (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-07-24
    Description: Most species' sex chromosomes are derived from ancient autosomes and show few signatures of their origins. We studied the sex chromosomes of Drosophila miranda, where a neo-Y chromosome originated only approximately 1 million years ago. Whole-genome and transcriptome analysis reveals massive degeneration of the neo-Y, that male-beneficial genes on the neo-Y are more likely to undergo accelerated protein evolution, and that neo-Y genes evolve biased expression toward male-specific tissues--the shrinking gene content of the neo-Y becomes masculinized. In contrast, although older X chromosomes show a paucity of genes expressed in male tissues, neo-X genes highly expressed in male-specific tissues undergo increased rates of protein evolution if haploid in males. Thus, the response to sex-specific selection can shift at different stages of X differentiation, resulting in masculinization or demasculinization of the X-chromosomal gene content.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4107656/" 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/PMC4107656/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, Qi -- Bachtrog, Doris -- R01 GM076007/GM/NIGMS NIH HHS/ -- R01 GM093182/GM/NIGMS NIH HHS/ -- R01GM076007/GM/NIGMS NIH HHS/ -- R01GM093182/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2012 Jul 20;337(6092):341-5. doi: 10.1126/science.1225385.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Integrative Biology, 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/22822149" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological/*genetics ; Animals ; Drosophila/genetics/*physiology ; *Evolution, Molecular ; Female ; Gene Expression Regulation ; *Genes, Insect ; Genome-Wide Association Study ; Male ; Mutation ; Open Reading Frames ; Sex Factors ; Testis ; X Chromosome/*genetics ; Y Chromosome/*genetics
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    A histone acetyltransferase regulates active DNA demethylation in Arabidopsis (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-06-16
    Description: Active DNA demethylation is an important part of epigenetic regulation in plants and animals. How active DNA demethylation is regulated and its relationship with histone modification patterns are unclear. Here, we report the discovery of IDM1, a regulator of DNA demethylation in Arabidopsis. IDM1 is required for preventing DNA hypermethylation of highly homologous multicopy genes and other repetitive sequences that are normally targeted for active DNA demethylation by Repressor of Silencing 1 and related 5-methylcytosine DNA glycosylases. IDM1 binds methylated DNA at chromatin sites lacking histone H3K4 di- or trimethylation and acetylates H3 to create a chromatin environment permissible for 5-methylcytosine DNA glycosylases to function. Our study reveals how some genes are indicated by multiple epigenetic marks for active DNA demethylation and protection from silencing.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3575687/" 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/PMC3575687/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Qian, Weiqiang -- Miki, Daisuke -- Zhang, Heng -- Liu, Yunhua -- Zhang, Xi -- Tang, Kai -- Kan, Yunchao -- La, Honggui -- Li, Xiaojie -- Li, Shaofang -- Zhu, Xiaohong -- Shi, Xiaobing -- Zhang, Kangling -- Pontes, Olga -- Chen, Xuemei -- Liu, Renyi -- Gong, Zhizhong -- Zhu, Jian-Kang -- R01 GM059138/GM/NIGMS NIH HHS/ -- R01 GM070795/GM/NIGMS NIH HHS/ -- R01GM059138/GM/NIGMS NIH HHS/ -- R01GM070795/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2012 Jun 15;336(6087):1445-8. doi: 10.1126/science.1219416.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Shanghai Center for Plant Stress Biology and Shanghai Institute of Plant Physiology and Ecology, Shanghai Institutes of Biological Sciences, Chinese Academy of Sciences, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22700931" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Arabidopsis/*genetics/*metabolism ; Arabidopsis Proteins/chemistry/genetics/*metabolism ; Chromatin/metabolism ; DNA Glycosylases/metabolism ; *DNA Methylation ; DNA, Plant/*metabolism ; Gene Silencing ; Genes, Plant ; Histone Acetyltransferases/chemistry/genetics/*metabolism ; Histones/metabolism ; Methylation ; Mutation ; Nuclear Proteins/genetics/metabolism ; Protein Structure, Tertiary ; Transgenes
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    Processing and subcellular trafficking of ER-tethered EIN2 control response to ethylene gas (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-09-01
    Description: Ethylene gas is essential for many developmental processes and stress responses in plants. ETHYLENE INSENSITIVE2 (EIN2), an NRAMP-like integral membrane protein, plays an essential role in ethylene signaling, but its function remains enigmatic. Here we report that phosphorylation-regulated proteolytic processing of EIN2 triggers its endoplasmic reticulum (ER)-to-nucleus translocation. ER-tethered EIN2 shows CONSTITUTIVE TRIPLE RESPONSE1 (CTR1) kinase-dependent phosphorylation. Ethylene triggers dephosphorylation at several sites and proteolytic cleavage at one of these sites, resulting in nuclear translocation of a carboxyl-terminal EIN2 fragment (EIN2-C'). Mutations that mimic EIN2 dephosphorylation, or inactivate CTR1, show constitutive cleavage and nuclear localization of EIN2-C' and EIN3 and EIN3-LIKE1-dependent activation of ethylene responses. These findings uncover a mechanism of subcellular communication whereby ethylene stimulates phosphorylation-dependent cleavage and nuclear movement of the EIN2-C' peptide, linking hormone perception and signaling components in the ER with nuclear-localized transcriptional regulators.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3523706/" 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/PMC3523706/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Qiao, Hong -- Shen, Zhouxin -- Huang, Shao-shan Carol -- Schmitz, Robert J -- Urich, Mark A -- Briggs, Steven P -- Ecker, Joseph R -- F32 HG004830/HG/NHGRI NIH HHS/ -- F32-HG004830/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Oct 19;338(6105):390-3. doi: 10.1126/science.1225974. Epub 2012 Aug 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Plant Biology Laboratory, Salk Institute for Biological Studies, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22936567" target="_blank"〉PubMed〈/a〉
    Keywords: Active Transport, Cell Nucleus ; Arabidopsis/drug effects/*metabolism ; Arabidopsis Proteins/genetics/*metabolism ; Cell Nucleus/*metabolism ; Endoplasmic Reticulum/*metabolism ; Ethylenes/*metabolism/pharmacology ; Gases/metabolism/pharmacology ; Mutation ; Nuclear Localization Signals/genetics/metabolism ; Phosphorylation ; Protein Kinases/metabolism ; Proteolysis ; Receptors, Cell Surface/genetics/*metabolism
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    Coagulation factor X activates innate immunity to human species C adenovirus (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-09-29
    Description: Although coagulation factors play a role in host defense for "living fossils" such as horseshoe crabs, the role of the coagulation system in immunity in higher organisms remains unclear. We modeled the interface of human species C adenovirus (HAdv) interaction with coagulation factor X (FX) and introduced a mutation that abrogated formation of the HAdv-FX complex. In vivo genome-wide transcriptional profiling revealed that FX-binding-ablated virus failed to activate a distinct network of nuclear factor kappaB-dependent early-response genes that are activated by HAdv-FX complex downstream of TLR4/MyD88/TRIF/TRAF6 signaling. Our study implicates host factor "decoration" of the virus as a mechanism to trigger an innate immune sensor that responds to a misplacement of coagulation FX from the blood into intracellular macrophage compartments upon virus entry into the cell.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4762479/" 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/PMC4762479/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Doronin, Konstantin -- Flatt, Justin W -- Di Paolo, Nelson C -- Khare, Reeti -- Kalyuzhniy, Oleksandr -- Acchione, Mauro -- Sumida, John P -- Ohto, Umeharu -- Shimizu, Toshiyuki -- Akashi-Takamura, Sachiko -- Miyake, Kensuke -- MacDonald, James W -- Bammler, Theo K -- Beyer, Richard P -- Farin, Frederico M -- Stewart, Phoebe L -- Shayakhmetov, Dmitry M -- AI065429/AI/NIAID NIH HHS/ -- CA141439/CA/NCI NIH HHS/ -- P30ES07033/ES/NIEHS NIH HHS/ -- R01 AI065429/AI/NIAID NIH HHS/ -- R01 CA141439/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2012 Nov 9;338(6108):795-8. doi: 10.1126/science.1226625. Epub 2012 Sep 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Washington, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23019612" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae Infections/*immunology/metabolism/virology ; Adenoviruses, Human/genetics/*immunology/*metabolism ; Animals ; CHO Cells ; Capsid Proteins/chemistry/genetics/metabolism ; Cell Line, Tumor ; Cricetinae ; Cricetulus ; Cryoelectron Microscopy ; Cytokines/metabolism ; Factor X/chemistry/*metabolism ; Gene Expression Profiling ; Gene Expression Regulation ; Hepatocytes/virology ; Humans ; *Immunity, Innate ; Macrophages/metabolism/virology ; Mice ; Mice, Inbred C57BL ; Molecular Dynamics Simulation ; Mutation ; NF-kappa B/metabolism ; Signal Transduction ; Virus Internalization
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    Real-time evolution of new genes by innovation, amplification, and divergence (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-10-23
    Description: Gene duplications allow evolution of genes with new functions. Here, we describe the innovation-amplification-divergence (IAD) model in which the new function appears before duplication and functionally distinct new genes evolve under continuous selection. One example fitting this model is a preexisting parental gene in Salmonella enterica that has low levels of two distinct activities. This gene is amplified to a high copy number, and the amplified gene copies accumulate mutations that provide enzymatic specialization of different copies and faster growth. Selection maintains the initial amplification and beneficial mutant alleles but is relaxed for other less improved gene copies, allowing their loss. This rapid process, completed in fewer than 3000 generations, shows the efficacy of the IAD model and allows the study of gene evolution in real time.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4392837/" 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/PMC4392837/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nasvall, Joakim -- Sun, Lei -- Roth, John R -- Andersson, Dan I -- GM27068/GM/NIGMS NIH HHS/ -- R01 GM027068/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2012 Oct 19;338(6105):384-7. doi: 10.1126/science.1226521.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Biochemistry and Microbiology, Uppsala University, Uppsala, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23087246" target="_blank"〉PubMed〈/a〉
    Keywords: *Evolution, Molecular ; *Gene Amplification ; Gene Dosage ; *Genetic Variation ; Histidine/genetics ; *Models, Genetic ; Mutation ; Salmonella enterica/*genetics ; Selection, Genetic ; Time
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    Dystroglycan function requires xylosyl- and glucuronyltransferase activities of LARGE (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-01-10
    Description: Posttranslational modification of alpha-dystroglycan (alpha-DG) by the like-acetylglucosaminyltransferase (LARGE) is required for it to function as an extracellular matrix (ECM) receptor. Mutations in the LARGE gene have been identified in congenital muscular dystrophy patients with brain abnormalities. However, the precise function of LARGE remains unclear. Here we found that LARGE could act as a bifunctional glycosyltransferase, with both xylosyltransferase and glucuronyltransferase activities, which produced repeating units of [-3-xylose-alpha1,3-glucuronic acid-beta1-]. This modification allowed alpha-DG to bind laminin-G domain-containing ECM ligands.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3702376/" 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/PMC3702376/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Inamori, Kei-ichiro -- Yoshida-Moriguchi, Takako -- Hara, Yuji -- Anderson, Mary E -- Yu, Liping -- Campbell, Kevin P -- 1U54NS053672/NS/NINDS NIH HHS/ -- U54 NS053672/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Jan 6;335(6064):93-6. doi: 10.1126/science.1214115.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Molecular Physiology and Biophysics, University of Iowa Roy J. and Lucille A. Carver College of Medicine, 4283 Carver Biomedical Research Building, 285 Newton Road, Iowa City, IA 52242-1101, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22223806" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Animals ; CHO Cells ; Carbohydrate Conformation ; Catalytic Domain ; Cricetinae ; Dystroglycans/chemistry/*metabolism ; Glucuronic Acid/metabolism ; Glucuronosyltransferase/metabolism ; Glycosaminoglycans/metabolism ; Glycosylation ; HEK293 Cells ; Humans ; Laminin/metabolism ; Ligands ; Mice ; Mutation ; N-Acetylglucosaminyltransferases/chemistry/genetics/*metabolism ; Pentosyltransferases/metabolism ; Polysaccharides/*metabolism ; Protein Processing, Post-Translational ; Recombinant Proteins/metabolism ; Xylose/metabolism
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    MORC family ATPases required for heterochromatin condensation and gene silencing (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-05-05
    Description: Transposable elements (TEs) and DNA repeats are commonly targeted by DNA and histone methylation to achieve epigenetic gene silencing. We isolated mutations in two Arabidopsis genes, AtMORC1 and AtMORC6, which cause derepression of DNA-methylated genes and TEs but no losses of DNA or histone methylation. AtMORC1 and AtMORC6 are members of the conserved Microrchidia (MORC) adenosine triphosphatase (ATPase) family, which are predicted to catalyze alterations in chromosome superstructure. The atmorc1 and atmorc6 mutants show decondensation of pericentromeric heterochromatin, increased interaction of pericentromeric regions with the rest of the genome, and transcriptional defects that are largely restricted to loci residing in pericentromeric regions. Knockdown of the single MORC homolog in Caenorhabditis elegans also impairs transgene silencing. We propose that the MORC ATPases are conserved regulators of gene silencing in eukaryotes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3376212/" 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/PMC3376212/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moissiard, Guillaume -- Cokus, Shawn J -- Cary, Joshua -- Feng, Suhua -- Billi, Allison C -- Stroud, Hume -- Husmann, Dylan -- Zhan, Ye -- Lajoie, Bryan R -- McCord, Rachel Patton -- Hale, Christopher J -- Feng, Wei -- Michaels, Scott D -- Frand, Alison R -- Pellegrini, Matteo -- Dekker, Job -- Kim, John K -- Jacobsen, Steven E -- F32 GM100617/GM/NIGMS NIH HHS/ -- F32GM100617/GM/NIGMS NIH HHS/ -- GM007185/GM/NIGMS NIH HHS/ -- GM075060/GM/NIGMS NIH HHS/ -- GM088565/GM/NIGMS NIH HHS/ -- GM60398/GM/NIGMS NIH HHS/ -- HG003143/HG/NHGRI NIH HHS/ -- R01 GM075060/GM/NIGMS NIH HHS/ -- R01 GM088565/GM/NIGMS NIH HHS/ -- R01 HG003143/HG/NHGRI NIH HHS/ -- R37 GM060398/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Jun 15;336(6087):1448-51. doi: 10.1126/science.1221472. Epub 2012 May 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular, Cell, and Developmental Biology, University of California at Los Angeles, Terasaki Life Sciences Building, 610 Charles Young Drive East, Los Angeles, CA 90095-723905, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22555433" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphatases/chemistry/genetics/*metabolism ; Animals ; Arabidopsis/enzymology/*genetics/*metabolism ; Arabidopsis Proteins/chemistry/genetics/*metabolism ; Caenorhabditis elegans ; Caenorhabditis elegans Proteins/genetics/metabolism ; Centromere ; DNA Methylation ; DNA Transposable Elements ; *Gene Silencing ; Genes, Plant ; Heterochromatin/*metabolism/ultrastructure ; Histones/metabolism ; Methylation ; Mutation ; RNA, Small Interfering/metabolism ; Transcription, Genetic ; Transgenes ; Up-Regulation
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    Cost-benefit tradeoffs in engineered lac operons (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-05-19
    Description: Cells must balance the cost and benefit of protein expression to optimize organismal fitness. The lac operon of the bacterium Escherichia coli has been a model for quantifying the physiological impact of costly protein production and for elucidating the resulting regulatory mechanisms. We report quantitative fitness measurements in 27 redesigned operons that suggested that protein production is not the primary origin of fitness costs. Instead, we discovered that the lac permease activity, which relates linearly to cost, is the major physiological burden to the cell. These findings explain control points in the lac operon that minimize the cost of lac permease activity, not protein expression. Characterizing similar relationships in other systems will be important to map the impact of cost/benefit tradeoffs on cell physiology and regulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eames, Matt -- Kortemme, Tanja -- New York, N.Y. -- Science. 2012 May 18;336(6083):911-5. doi: 10.1126/science.1219083.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate Group in Biophysics, MC 2530, University of California, San Francisco, CA 94158-2330, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22605776" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Biocatalysis ; Biological Transport ; Escherichia coli/*genetics/growth & development/metabolism ; Escherichia coli Proteins/*genetics/*metabolism ; Gene Expression Regulation, Bacterial ; Gene Knockout Techniques ; Genetic Engineering ; Isopropyl Thiogalactoside/metabolism ; *Lac Operon ; Lac Repressors ; Lactose/metabolism ; Models, Biological ; Molecular Sequence Data ; Monosaccharide Transport Proteins/*genetics/*metabolism ; Mutation ; Symporters/*genetics/*metabolism ; beta-Galactosidase/*genetics/*metabolism
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    Neurexin and neuroligin mediate retrograde synaptic inhibition in C. elegans (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-08-04
    Description: The synaptic adhesion molecules neurexin and neuroligin alter the development and function of synapses and are linked to autism in humans. Here, we found that Caenorhabditis elegans neurexin (NRX-1) and neuroligin (NLG-1) mediated a retrograde synaptic signal that inhibited neurotransmitter release at neuromuscular junctions. Retrograde signaling was induced in mutants lacking a muscle microRNA (miR-1) and was blocked in mutants lacking NLG-1 or NRX-1. Release was rapid and abbreviated when the retrograde signal was on, whereas release was slow and prolonged when retrograde signaling was blocked. The retrograde signal adjusted release kinetics by inhibiting exocytosis of synaptic vesicles (SVs) that are distal to the site of calcium entry. Inhibition of release was mediated by increased presynaptic levels of tomosyn, an inhibitor of SV fusion.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3791080/" 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/PMC3791080/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hu, Zhitao -- Hom, Sabrina -- Kudze, Tambudzai -- Tong, Xia-Jing -- Choi, Seungwon -- Aramuni, Gayane -- Zhang, Weiqi -- Kaplan, Joshua M -- NS32196/NS/NINDS NIH HHS/ -- R37 NS032196/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2012 Aug 24;337(6097):980-4. doi: 10.1126/science.1224896. Epub 2012 Aug 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22859820" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/metabolism ; Animals ; Caenorhabditis elegans/genetics/*physiology ; Caenorhabditis elegans Proteins/genetics/*metabolism ; Cell Adhesion Molecules, Neuronal/genetics/*metabolism ; Cholinergic Neurons/physiology ; Excitatory Postsynaptic Potentials ; Exocytosis ; Kinetics ; Mice ; MicroRNAs/genetics/metabolism ; Motor Neurons/physiology ; Mutation ; Neural Inhibition ; Neuromuscular Junction/*physiology ; Neurotransmitter Agents/metabolism ; *Synaptic Transmission ; Synaptic Vesicles/physiology ; Transcription Factors/genetics/metabolism ; Transfection
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    Landscape of somatic retrotransposition in human cancers (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-30
    Description: Transposable elements (TEs) are abundant in the human genome, and some are capable of generating new insertions through RNA intermediates. In cancer, the disruption of cellular mechanisms that normally suppress TE activity may facilitate mutagenic retrotranspositions. We performed single-nucleotide resolution analysis of TE insertions in 43 high-coverage whole-genome sequencing data sets from five cancer types. We identified 194 high-confidence somatic TE insertions, as well as thousands of polymorphic TE insertions in matched normal genomes. Somatic insertions were present in epithelial tumors but not in blood or brain cancers. Somatic L1 insertions tend to occur in genes that are commonly mutated in cancer, disrupt the expression of the target genes, and are biased toward regions of cancer-specific DNA hypomethylation, highlighting their potential impact in tumorigenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3656569/" 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/PMC3656569/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Eunjung -- Iskow, Rebecca -- Yang, Lixing -- Gokcumen, Omer -- Haseley, Psalm -- Luquette, Lovelace J 3rd -- Lohr, Jens G -- Harris, Christopher C -- Ding, Li -- Wilson, Richard K -- Wheeler, David A -- Gibbs, Richard A -- Kucherlapati, Raju -- Lee, Charles -- Kharchenko, Peter V -- Park, Peter J -- Cancer Genome Atlas Research Network -- F32 AG039979/AG/NIA NIH HHS/ -- F32AG039979/AG/NIA NIH HHS/ -- K25 AG037596/AG/NIA NIH HHS/ -- K25AG037596/AG/NIA NIH HHS/ -- R01 GM082798/GM/NIGMS NIH HHS/ -- R01GM082798/GM/NIGMS NIH HHS/ -- RC1HG005482/HG/NHGRI NIH HHS/ -- T32 CA009172/CA/NCI NIH HHS/ -- U01 HG005725/HG/NHGRI NIH HHS/ -- U01HG005209/HG/NHGRI NIH HHS/ -- U01HG005725/HG/NHGRI NIH HHS/ -- U24 CA144025/CA/NCI NIH HHS/ -- U24CA144025/CA/NCI NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2012 Aug 24;337(6097):967-71. doi: 10.1126/science.1222077. Epub 2012 Jun 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Biomedical Informatics, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22745252" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Cell Transformation, Neoplastic ; Colorectal Neoplasms/*genetics ; DNA Methylation ; Female ; Gene Expression Regulation, Neoplastic ; Genes, Neoplasm ; Genome, Human ; Glioblastoma/*genetics ; Humans ; Long Interspersed Nucleotide Elements ; Male ; Microsatellite Instability ; Molecular Sequence Annotation ; Molecular Sequence Data ; Multiple Myeloma/*genetics ; Mutagenesis, Insertional ; Mutation ; Ovarian Neoplasms/*genetics ; Prostatic Neoplasms/*genetics ; *Retroelements ; Sequence Analysis, DNA
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    Physico-genetic determinants in the evolution of development (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-10-16
    Description: Animal bodies and the embryos that generate them exhibit an assortment of stereotypic morphological motifs that first appeared more than half a billion years ago. During development, cells arrange themselves into tissues with interior cavities and multiple layers with immiscible boundaries, containing patterned arrangements of cell types. These tissues go on to elongate, fold, segment, and form appendages. Their motifs are similar to the outcomes of physical processes generic to condensed, chemically excitable, viscoelastic materials, although the embryonic mechanisms that generate them are typically much more complex. I propose that the origins of animal development lay in the mobilization of physical organizational effects that resulted when certain gene products of single-celled ancestors came to operate on the spatial scale of multicellular aggregates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Newman, Stuart A -- New York, N.Y. -- Science. 2012 Oct 12;338(6104):217-9. doi: 10.1126/science.1222003.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology and Anatomy, New York Medical College, Valhalla, NY 10595, USA. newman@nymc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23066074" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Body Patterning/*genetics ; Chimerism/embryology ; Cleavage Stage, Ovum ; Invertebrates/embryology ; Mutation ; Physical Phenomena ; *Physical Processes ; Vertebrates/embryology
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    AIDS/HIV. HIV interplay with SAMHD1 (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-03-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schaller, Torsten -- Goujon, Caroline -- Malim, Michael H -- G0401570/Medical Research Council/United Kingdom -- G1000196/Medical Research Council/United Kingdom -- G1001081/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2012 Mar 16;335(6074):1313-4. doi: 10.1126/science.1221057.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Infectious Diseases, King's College London School of Medicine, Guy's Hospital, London, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22422971" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptive Immunity ; Animals ; Autoimmune Diseases of the Nervous System/genetics ; DNA, Complementary/metabolism ; Genes, Viral ; HIV Infections/immunology/*virology ; HIV-1/*immunology/pathogenicity/*physiology ; HIV-2/pathogenicity ; Humans ; Immunity, Innate ; Monomeric GTP-Binding Proteins/chemistry/genetics/*metabolism ; Mutation ; Myeloid Cells/*virology ; Nervous System Malformations/genetics ; Nucleotides/metabolism ; Simian Immunodeficiency Virus/pathogenicity ; Viral Regulatory and Accessory Proteins/genetics/metabolism ; Virus Replication
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    Chloroplast biogenesis is regulated by direct action of the ubiquitin-proteasome system (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-11-03
    Description: Development of chloroplasts and other plastids depends on the import of thousands of nucleus-encoded proteins from the cytosol. Import is initiated by TOC (translocon at the outer envelope of chloroplasts) complexes in the plastid outer membrane that incorporate multiple, client-specific receptors. Modulation of import is thought to control the plastid's proteome, developmental fate, and functions. Using forward genetics, we identified Arabidopsis SP1, which encodes a RING-type ubiquitin E3 ligase of the chloroplast outer membrane. The SP1 protein associated with TOC complexes and mediated ubiquitination of TOC components, promoting their degradation. Mutant sp1 plants performed developmental transitions that involve plastid proteome changes inefficiently, indicating a requirement for reorganization of the TOC machinery. Thus, the ubiquitin-proteasome system acts on plastids to control their development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ling, Qihua -- Huang, Weihua -- Baldwin, Amy -- Jarvis, Paul -- BB/D016541/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/H008039/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- New York, N.Y. -- Science. 2012 Nov 2;338(6107):655-9. doi: 10.1126/science.1225053.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of Leicester, Leicester LE1 7RH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23118188" target="_blank"〉PubMed〈/a〉
    Keywords: Apoptosis Regulatory Proteins/chemistry/*genetics/*metabolism ; Arabidopsis/genetics/growth & development/*metabolism/ultrastructure ; Arabidopsis Proteins/chemistry/*genetics/*metabolism ; Chloroplast Proteins/*metabolism ; Chloroplasts/*metabolism/ultrastructure ; Membrane Proteins/genetics/metabolism ; Mutation ; Proteasome Endopeptidase Complex/*metabolism ; Protein Precursors/genetics/metabolism ; Protein Transport ; Proteome ; RING Finger Domains ; Ubiquitin-Protein Ligases/chemistry/*genetics/*metabolism ; Ubiquitination
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    Evolution, safety, and highly pathogenic influenza viruses (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-23
    Description: Experience with influenza has shown that predictions of virus phenotype or fitness from nucleotide sequence are imperfect and that predicting the timing and course of evolution is extremely difficult. Such uncertainty means that the risk of experiments with mammalian-transmissible, possibly highly virulent influenza viruses remains high even if some aspects of their laboratory biology are reassuring; it also implies limitations on the ability of laboratory observations to guide interpretation of surveillance of strains in the field. Thus, we propose that future experiments with virulent pathogens whose accidental or deliberate release could lead to extensive spread in human populations should be limited by explicit risk-benefit considerations.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3467308/" 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/PMC3467308/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lipsitch, Marc -- Plotkin, Joshua B -- Simonsen, Lone -- Bloom, Barry -- U54 GM088558/GM/NIGMS NIH HHS/ -- U54GM088558/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2012 Jun 22;336(6088):1529-31. doi: 10.1126/science.1223204.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Communicable Disease Dynamics and Department of Epidemiology, Harvard School of Public Health, Boston, MA 02115, USA. mlipsitc@hsph.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22723411" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigenic Variation ; Antigens, Viral ; Antiviral Agents/pharmacology/therapeutic use ; Biohazard Release ; *Containment of Biohazards ; Drug Resistance, Viral ; *Evolution, Molecular ; Ferrets ; Humans ; Influenza A Virus, H5N1 Subtype/genetics/*pathogenicity ; Influenza A virus/drug effects/genetics/immunology/*pathogenicity ; Influenza, Human/drug therapy/transmission/*virology ; Laboratory Infection/epidemiology ; Mutation ; Orthomyxoviridae Infections/transmission/*virology ; Public Policy ; Risk Assessment ; *Safety ; Security Measures ; United States/epidemiology
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    Evolutionarily assembled cis-regulatory module at a human ciliopathy locus (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-01-28
    Description: Neighboring genes are often coordinately expressed within cis-regulatory modules, but evidence that nonparalogous genes share functions in mammals is lacking. Here, we report that mutation of either TMEM138 or TMEM216 causes a phenotypically indistinguishable human ciliopathy, Joubert syndrome. Despite a lack of sequence homology, the genes are aligned in a head-to-tail configuration and joined by chromosomal rearrangement at the amphibian-to-reptile evolutionary transition. Expression of the two genes is mediated by a conserved regulatory element in the noncoding intergenic region. Coordinated expression is important for their interdependent cellular role in vesicular transport to primary cilia. Hence, during vertebrate evolution of genes involved in ciliogenesis, nonparalogous genes were arranged to a functional gene cluster with shared regulatory elements.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3671610/" 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/PMC3671610/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Jeong Ho -- Silhavy, Jennifer L -- Lee, Ji Eun -- Al-Gazali, Lihadh -- Thomas, Sophie -- Davis, Erica E -- Bielas, Stephanie L -- Hill, Kiley J -- Iannicelli, Miriam -- Brancati, Francesco -- Gabriel, Stacey B -- Russ, Carsten -- Logan, Clare V -- Sharif, Saghira Malik -- Bennett, Christopher P -- Abe, Masumi -- Hildebrandt, Friedhelm -- Diplas, Bill H -- Attie-Bitach, Tania -- Katsanis, Nicholas -- Rajab, Anna -- Koul, Roshan -- Sztriha, Laszlo -- Waters, Elizabeth R -- Ferro-Novick, Susan -- Woods, C Geoffrey -- Johnson, Colin A -- Valente, Enza Maria -- Zaki, Maha S -- Gleeson, Joseph G -- DK068306/DK/NIDDK NIH HHS/ -- DK072301/DK/NIDDK NIH HHS/ -- DK075972/DK/NIDDK NIH HHS/ -- DK090917/DK/NIDDK NIH HHS/ -- EY021872/EY/NEI NIH HHS/ -- G0700073/Medical Research Council/United Kingdom -- GGP08145/Telethon/Italy -- HD042601/HD/NICHD NIH HHS/ -- NS04843/NS/NINDS NIH HHS/ -- NS052455/NS/NINDS NIH HHS/ -- P30 CA023100/CA/NCI NIH HHS/ -- P30NS047101/NS/NINDS NIH HHS/ -- R01 DK068306/DK/NIDDK NIH HHS/ -- R01 DK072301/DK/NIDDK NIH HHS/ -- R01 DK075972/DK/NIDDK NIH HHS/ -- R01 EY021872/EY/NEI NIH HHS/ -- R01 HD042601/HD/NICHD NIH HHS/ -- R01 NS048453/NS/NINDS NIH HHS/ -- R01 NS052455/NS/NINDS NIH HHS/ -- U54 HG003067/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Feb 24;335(6071):966-9. doi: 10.1126/science.1213506. Epub 2012 Jan 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurogenetics Laboratory, Howard Hughes Medical Institute (HHMI), Department of Neurosciences, University of California, San Diego, CA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22282472" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; Cerebellar Diseases/*genetics/metabolism/pathology ; Cilia/metabolism/*ultrastructure ; Conserved Sequence ; DNA, Intergenic ; *Evolution, Molecular ; Eye Abnormalities/*genetics/metabolism/pathology ; Gene Expression Profiling ; *Gene Expression Regulation ; Genetic Heterogeneity ; *Genetic Loci ; Humans ; Kidney Diseases, Cystic/*genetics/metabolism/pathology ; Membrane Proteins/chemistry/*genetics/metabolism ; Molecular Sequence Data ; Multigene Family ; Mutation ; Mutation, Missense ; Phenotype ; Protein Transport ; *Regulatory Sequences, Nucleic Acid ; Retina/abnormalities/metabolism/pathology ; Transport Vesicles/metabolism/ultrastructure
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    Cotranscriptional role for Arabidopsis DICER-LIKE 4 in transcription termination (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-31
    Description: Transcription termination is emerging as an important component of gene regulation necessary to partition the genome and minimize transcriptional interference. We have discovered a role for the Arabidopsis RNA silencing enzyme DICER-LIKE 4 (DCL4) in transcription termination of an endogenous Arabidopsis gene, FCA. DCL4 directly associates with FCA chromatin in the 3' region and promotes cleavage of the nascent transcript in a domain downstream of the canonical polyA site. In a dcl4 mutant, the resulting transcriptional read-through triggers an RNA interference-mediated gene silencing of a transgene containing the same 3' region. We conclude that DCL4 promotes transcription termination of the Arabidopsis FCA gene, reducing the amount of aberrant RNA produced from the locus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Fuquan -- Bakht, Saleha -- Dean, Caroline -- BB/D010799/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/G01406X/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- New York, N.Y. -- Science. 2012 Mar 30;335(6076):1621-3. doi: 10.1126/science.1214402.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Developmental Biology, John Innes Centre, Norwich Research Park, Norwich, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22461611" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/*genetics/metabolism ; Arabidopsis Proteins/*genetics/metabolism ; Base Sequence ; Chromatin/genetics/metabolism ; Chromatin Immunoprecipitation ; *Gene Expression Regulation, Plant ; MADS Domain Proteins/genetics/metabolism ; Molecular Sequence Data ; Mutation ; Polyadenylation ; Protein Structure, Tertiary ; RNA Interference ; RNA, Messenger/genetics/metabolism ; RNA, Plant/*genetics/metabolism ; RNA-Binding Proteins/*genetics/metabolism ; Ribonuclease III/chemistry/genetics/*metabolism ; *Transcription, Genetic ; Transgenes
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    The potential for respiratory droplet-transmissible A/H5N1 influenza virus to evolve in a mammalian host (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-23
    Description: Avian A/H5N1 influenza viruses pose a pandemic threat. As few as five amino acid substitutions, or four with reassortment, might be sufficient for mammal-to-mammal transmission through respiratory droplets. From surveillance data, we found that two of these substitutions are common in A/H5N1 viruses, and thus, some viruses might require only three additional substitutions to become transmissible via respiratory droplets between mammals. We used a mathematical model of within-host virus evolution to study factors that could increase and decrease the probability of the remaining substitutions evolving after the virus has infected a mammalian host. These factors, combined with the presence of some of these substitutions in circulating strains, make a virus evolving in nature a potentially serious threat. These results highlight critical areas in which more data are needed for assessing, and potentially averting, this threat.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3426314/" 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/PMC3426314/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Russell, Colin A -- Fonville, Judith M -- Brown, Andre E X -- Burke, David F -- Smith, David L -- James, Sarah L -- Herfst, Sander -- van Boheemen, Sander -- Linster, Martin -- Schrauwen, Eefje J -- Katzelnick, Leah -- Mosterin, Ana -- Kuiken, Thijs -- Maher, Eileen -- Neumann, Gabriele -- Osterhaus, Albert D M E -- Kawaoka, Yoshihiro -- Fouchier, Ron A M -- Smith, Derek J -- DP1 OD000490/OD/NIH HHS/ -- DP1-OD000490-01/OD/NIH HHS/ -- HHSN266200700010C/AI/NIAID NIH HHS/ -- HHSN266200700010C/PHS HHS/ -- R01 AI 069274/AI/NIAID NIH HHS/ -- R56 AI069274/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2012 Jun 22;336(6088):1541-7. doi: 10.1126/science.1222526.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Zoology, University of Cambridge, Cambridge, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22723414" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; Air Microbiology ; Amino Acid Substitution ; Animals ; Birds ; *Evolution, Molecular ; Genetic Fitness ; Glycosylation ; Hemagglutinin Glycoproteins, Influenza Virus/*genetics/metabolism ; High-Throughput Nucleotide Sequencing ; Humans ; Influenza A Virus, H5N1 Subtype/*genetics/*pathogenicity ; Influenza in Birds/virology ; Influenza, Human/immunology/transmission/*virology ; Mammals ; Models, Biological ; Mutation ; Orthomyxoviridae Infections/transmission/*virology ; Probability ; RNA Replicase/*genetics ; Receptors, Virus/metabolism ; Respiratory System/*virology ; Selection, Genetic ; Sialic Acids/metabolism ; Viral Proteins/*genetics
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    Molecular biology. Genetic events that shape the cancer epigenome (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ryan, Russell J H -- Bernstein, Bradley E -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Jun 22;336(6088):1513-4. doi: 10.1126/science.1223730.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Pathology and Center for Cancer Research, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22723401" target="_blank"〉PubMed〈/a〉
    Keywords: Chromatin/chemistry/*metabolism/ultrastructure ; DNA Methylation ; Enhancer Elements, Genetic ; *Epigenesis, Genetic ; *Gene Expression Regulation, Neoplastic ; Gene Silencing ; *Genome, Human ; Histones/genetics/*metabolism ; Humans ; Methylation ; Mutation ; Neoplasms/*genetics/metabolism ; Promoter Regions, Genetic ; Transcription Factors/*metabolism ; *Transcription, Genetic
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    The path from beta-carotene to carlactone, a strigolactone-like plant hormone (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-17
    Description: Strigolactones, phytohormones with diverse signaling activities, have a common structure consisting of two lactones connected by an enol-ether bridge. Strigolactones derive from carotenoids via a pathway involving the carotenoid cleavage dioxygenases 7 and 8 (CCD7 and CCD8) and the iron-binding protein D27. We show that D27 is a beta-carotene isomerase that converts all-trans-beta-carotene into 9-cis-beta-carotene, which is cleaved by CCD7 into a 9-cis-configured aldehyde. CCD8 incorporates three oxygens into 9-cis-beta-apo-10'-carotenal and performs molecular rearrangement, linking carotenoids with strigolactones and producing carlactone, a compound with strigolactone-like biological activities. Knowledge of the structure of carlactone will be crucial for understanding the biology of strigolactones and may have applications in combating parasitic weeds.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alder, Adrian -- Jamil, Muhammad -- Marzorati, Mattia -- Bruno, Mark -- Vermathen, Martina -- Bigler, Peter -- Ghisla, Sandro -- Bouwmeester, Harro -- Beyer, Peter -- Al-Babili, Salim -- New York, N.Y. -- Science. 2012 Mar 16;335(6074):1348-51. doi: 10.1126/science.1218094.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Faculty of Biology, University of Freiburg, Freiburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22422982" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/genetics/*metabolism ; Arabidopsis Proteins/genetics/metabolism ; Biosynthetic Pathways ; Carotenoids/chemistry/metabolism ; Dioxygenases/genetics/metabolism ; Germination ; Isomerases/genetics/metabolism ; Lactones/chemistry/*metabolism/pharmacology ; Molecular Structure ; Mutation ; Oryza/genetics/*metabolism ; Peas/genetics/*metabolism ; Phenotype ; Plant Growth Regulators/*biosynthesis/chemistry ; Plant Proteins/genetics/metabolism ; Stereoisomerism ; Striga/growth & development ; beta Carotene/*metabolism
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    Function, targets, and evolution of Caenorhabditis elegans piRNAs (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-06-16
    Description: Piwi-interacting RNAs (piRNAs) are small RNAs required to maintain germline integrity and fertility, but their mechanism of action is poorly understood. Here we demonstrate that Caenorhabditis elegans piRNAs silence transcripts in trans through imperfectly complementary sites. Target silencing is independent of Piwi endonuclease activity or "slicing." Instead, piRNAs initiate a localized secondary endogenous small interfering RNA (endo-siRNA) response. Endogenous protein-coding gene and transposon transcripts exhibit Piwi-dependent endo-siRNAs at sites complementary to piRNAs and are derepressed in Piwi mutants. Genomic loci of piRNA biogenesis are depleted of protein-coding genes and tend to overlap the start and end of transposons in sense and antisense, respectively. Our data suggest that nematode piRNA clusters are evolving to generate piRNAs against active mobile elements. Thus, piRNAs provide heritable, sequence-specific triggers for RNA interference in C. elegans.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3951736/" 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/PMC3951736/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bagijn, Marloes P -- Goldstein, Leonard D -- Sapetschnig, Alexandra -- Weick, Eva-Maria -- Bouasker, Samir -- Lehrbach, Nicolas J -- Simard, Martin J -- Miska, Eric A -- 092096/Wellcome Trust/United Kingdom -- 11832/Cancer Research UK/United Kingdom -- A14492/Cancer Research UK/United Kingdom -- Wellcome Trust/United Kingdom -- Cancer Research UK/United Kingdom -- Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2012 Aug 3;337(6094):574-8. doi: 10.1126/science.1220952. Epub 2012 Jun 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gurdon Institute and Department of Biochemistry, University of Cambridge, The Henry Wellcome Building of Cancer and Developmental Biology, Tennis Court Road, Cambridge CB2 1QN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22700655" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Argonaute Proteins/genetics ; Caenorhabditis elegans/*genetics ; Caenorhabditis elegans Proteins/genetics ; Evolution, Molecular ; Mutation ; *RNA Interference ; RNA, Double-Stranded/biosynthesis/genetics ; RNA, Small Interfering/genetics/*metabolism ; *Transcription, Genetic
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    Influenza. One H5N1 paper finally goes to press; second greenlighted (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-05-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Enserink, Martin -- Cohen, Jon -- New York, N.Y. -- Science. 2012 May 4;336(6081):529-30. doi: 10.1126/science.336.6081.529.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22556223" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites/genetics ; Containment of Biohazards ; Ferrets ; Hemagglutinin Glycoproteins, Influenza Virus/chemistry/*genetics/metabolism ; Humans ; Influenza A Virus, H5N1 Subtype/genetics/*pathogenicity ; Influenza, Human/transmission/virology ; Mutation ; Orthomyxoviridae Infections/transmission/virology ; *Publishing ; Receptors, Virus/metabolism ; Virus Internalization
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    Mutations in BCKD-kinase lead to a potentially treatable form of autism with epilepsy (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-09-08
    Description: Autism spectrum disorders are a genetically heterogeneous constellation of syndromes characterized by impairments in reciprocal social interaction. Available somatic treatments have limited efficacy. We have identified inactivating mutations in the gene BCKDK (Branched Chain Ketoacid Dehydrogenase Kinase) in consanguineous families with autism, epilepsy, and intellectual disability. The encoded protein is responsible for phosphorylation-mediated inactivation of the E1alpha subunit of branched-chain ketoacid dehydrogenase (BCKDH). Patients with homozygous BCKDK mutations display reductions in BCKDK messenger RNA and protein, E1alpha phosphorylation, and plasma branched-chain amino acids. Bckdk knockout mice show abnormal brain amino acid profiles and neurobehavioral deficits that respond to dietary supplementation. Thus, autism presenting with intellectual disability and epilepsy caused by BCKDK mutations represents a potentially treatable syndrome.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3704165/" 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/PMC3704165/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Novarino, Gaia -- El-Fishawy, Paul -- Kayserili, Hulya -- Meguid, Nagwa A -- Scott, Eric M -- Schroth, Jana -- Silhavy, Jennifer L -- Kara, Majdi -- Khalil, Rehab O -- Ben-Omran, Tawfeg -- Ercan-Sencicek, A Gulhan -- Hashish, Adel F -- Sanders, Stephan J -- Gupta, Abha R -- Hashem, Hebatalla S -- Matern, Dietrich -- Gabriel, Stacey -- Sweetman, Larry -- Rahimi, Yasmeen -- Harris, Robert A -- State, Matthew W -- Gleeson, Joseph G -- K08 MH087639/MH/NIMH NIH HHS/ -- K08MH087639/MH/NIMH NIH HHS/ -- P01 HD070494/HD/NICHD NIH HHS/ -- P01HD070494/HD/NICHD NIH HHS/ -- P30 NS047101/NS/NINDS NIH HHS/ -- P30NS047101/NS/NINDS NIH HHS/ -- R01 NS041537/NS/NINDS NIH HHS/ -- R01 NS048453/NS/NINDS NIH HHS/ -- R01NS048453/NS/NINDS NIH HHS/ -- R25 MH077823/MH/NIMH NIH HHS/ -- RC2 MH089956/MH/NIMH NIH HHS/ -- RC2MH089956/MH/NIMH NIH HHS/ -- T32MH018268/MH/NIMH NIH HHS/ -- U54HG003067/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Oct 19;338(6105):394-7. doi: 10.1126/science.1224631. Epub 2012 Sep 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurogenetics Laboratory, Howard Hughes Medical Institute, Department of Neurosciences, University of California, San Diego, La Jolla, CA 92093, USA. gnovarino@ucsd.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22956686" target="_blank"〉PubMed〈/a〉
    Keywords: 3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)/*administration & ; dosage/deficiency/*genetics ; Adolescent ; Amino Acids, Branched-Chain/administration & dosage/blood/deficiency ; Animals ; Arginine/genetics ; Autistic Disorder/*diet therapy/enzymology/*genetics ; Base Sequence ; Brain/metabolism ; Child ; Child, Preschool ; Diet ; Epilepsy/*diet therapy/enzymology/*genetics ; Female ; Homozygote ; Humans ; Intellectual Disability/diet therapy/enzymology/genetics ; Male ; Mice ; Mice, Knockout ; Molecular Sequence Data ; Mutation ; Pedigree ; Phosphorylation ; Protein Folding ; Protein Structure, Tertiary ; RNA, Messenger/metabolism ; Young Adult
    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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    The fission yeast FANCM ortholog directs non-crossover recombination during meiosis (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-23
    Description: The formation of healthy gametes depends on programmed DNA double-strand breaks (DSBs), which are each repaired as a crossover (CO) or non-crossover (NCO) from a homologous template. Although most of these DSBs are repaired without giving COs, little is known about the genetic requirements of NCO-specific recombination. We show that Fml1, the Fanconi anemia complementation group M (FANCM)-ortholog of Schizosaccharomyces pombe, directs the formation of NCOs during meiosis in competition with the Mus81-dependent pro-CO pathway. We also define the Rad51/Dmc1-mediator Swi5-Sfr1 as a major determinant in biasing the recombination process in favor of Mus81, to ensure the appropriate amount of COs to guide meiotic chromosome segregation. The conservation of these proteins from yeast to humans suggests that this interplay may be a general feature of meiotic recombination.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3399777/" 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/PMC3399777/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lorenz, Alexander -- Osman, Fekret -- Sun, Weili -- Nandi, Saikat -- Steinacher, Roland -- Whitby, Matthew C -- 090767/Wellcome Trust/United Kingdom -- 090767/Z/09/Z/Wellcome Trust/United Kingdom -- J 2489/Austrian Science Fund FWF/Austria -- New York, N.Y. -- Science. 2012 Jun 22;336(6088):1585-8. doi: 10.1126/science.1220111.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Oxford, Oxford, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22723423" target="_blank"〉PubMed〈/a〉
    Keywords: Chromosome Segregation ; Chromosomes, Fungal/physiology ; *Crossing Over, Genetic ; DNA Breaks, Double-Stranded ; DNA Helicases/genetics/*metabolism ; DNA Repair ; DNA, Fungal/chemistry/metabolism ; DNA-Binding Proteins/genetics/metabolism ; Endonucleases/genetics/metabolism ; *Homologous Recombination ; *Meiosis ; Mutation ; Recombinases/genetics/metabolism ; Schizosaccharomyces/*genetics/physiology ; Schizosaccharomyces pombe Proteins/genetics/*metabolism
    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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    Type 6 secretion dynamics within and between bacterial cells (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-07-07
    Description: The bacterial type 6 secretion system (T6SS) functions as a virulence factor capable of attacking both eukaryotic and prokaryotic target cells by a process that involves protein transport through a contractile bacteriophage tail-like structure. The T6SS apparatus is composed, in part, of an exterior sheath wrapped around an interior tube. Here, we report that in living cells the cytoplasmic adenosine triphosphatase called ClpV specifically recognizes the contracted T6SS sheath structure, causing its disassembly within seconds. ClpV imaging allowed spatial and temporal documentation of cell-cell interactions (termed T6SS dueling) that likely mark the location of repeated T6SS-mediated protein translocation events between bacterial cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3557511/" 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/PMC3557511/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Basler, M -- Mekalanos, J J -- AI-018045/AI/NIAID NIH HHS/ -- AI-26289/AI/NIAID NIH HHS/ -- R01 AI018045/AI/NIAID NIH HHS/ -- R01 AI026289/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2012 Aug 17;337(6096):815. doi: 10.1126/science.1222901. Epub 2012 Jul 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunobiology, Harvard Medical School, 200 Longwood Avenue, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22767897" target="_blank"〉PubMed〈/a〉
    Keywords: Alanine/genetics/metabolism ; Amino Acid Substitution ; Bacterial Proteins/genetics/*metabolism ; *Bacterial Secretion Systems ; Green Fluorescent Proteins/genetics/metabolism ; Microscopy, Fluorescence/methods ; Molecular Imaging/methods ; Mutation ; Protein Transport ; Pseudomonas aeruginosa/metabolism/*physiology ; Recombinant Fusion Proteins/genetics/metabolism ; Tyrosine/genetics/metabolism ; Vibrio cholerae/metabolism/*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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    Immunology. Orchestrating inflammasomes (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-09-18
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4340476/" 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/PMC4340476/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Franchi, Luigi -- Nunez, Gabriel -- R01 DK091191/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2012 Sep 14;337(6100):1299-300. doi: 10.1126/science.1229010.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Comprehensive Cancer Center, University of Michigan Medical School, Ann Arbor, MI 48109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22984056" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CARD Signaling Adaptor Proteins/genetics/*metabolism ; Calcium-Binding Proteins/genetics/*metabolism ; Enzyme Activation ; Gram-Negative Bacteria/*immunology ; Gram-Negative Bacterial Infections/enzymology/*immunology ; Humans ; Inflammasomes/*metabolism ; Mice ; Mice, Mutant Strains ; Mutation ; Phosphorylation ; Protein Kinase C-delta/*metabolism ; Serine/genetics/metabolism
    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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    Multiple spectral inputs improve motion discrimination in the Drosophila visual system (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-05-19
    Description: Color and motion information are thought to be channeled through separate neural pathways, but it remains unclear whether and how these pathways interact to improve motion perception. In insects, such as Drosophila, it has long been believed that motion information is fed exclusively by one spectral class of photoreceptor, so-called R1 to R6 cells; whereas R7 and R8 photoreceptors, which exist in multiple spectral classes, subserve color vision. Here, we report that R7 and R8 also contribute to the motion pathway. By using electrophysiological, optical, and behavioral assays, we found that R7/R8 information converge with and shape the motion pathway output, explaining flies' broadly tuned optomotor behavior by its composite responses. Our results demonstrate that inputs from photoreceptors of different spectral sensitivities improve motion discrimination, increasing robustness of perception.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wardill, Trevor J -- List, Olivier -- Li, Xiaofeng -- Dongre, Sidhartha -- McCulloch, Marie -- Ting, Chun-Yuan -- O'Kane, Cahir J -- Tang, Shiming -- Lee, Chi-Hon -- Hardie, Roger C -- Juusola, Mikko -- BB/D007585/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/F012071/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/G006865/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/H013849/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2012 May 18;336(6083):925-31. doi: 10.1126/science.1215317.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biomedical Science, University of Sheffield, Sheffield S10 2TN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22605779" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Color Vision ; Drosophila Proteins ; Drosophila melanogaster/genetics/*physiology ; Flight, Animal ; Gap Junctions/physiology ; Genes, Insect ; Light ; Models, Neurological ; *Motion Perception ; Mutation ; Neurons/physiology ; Opsins/metabolism ; Optic Lobe, Nonmammalian/cytology/physiology ; Patch-Clamp Techniques ; Photoreceptor Cells, Invertebrate/*physiology/ultrastructure ; Transgenes ; Ultraviolet Rays ; Visual Pathways
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    Preventing Alzheimer's disease (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-09-22
    Description: Despite intensive laboratory and clinical research over three decades, an effective treatment to delay the onset and progression of Alzheimer's disease is not at hand. Recent clinical trial failures suggest that we must treat the disease earlier than in its mild to moderate stages, and major progress in validating presymptomatic biomarkers now makes secondary prevention trials possible. We will learn more about the natural history of the disease and any partial therapeutic responses from detailed analyses of recent trial results. This process will likely position the field for success, but only with much greater investment in all aspects of Alzheimer research and with careful design of future trials.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Selkoe, Dennis J -- New York, N.Y. -- Science. 2012 Sep 21;337(6101):1488-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. dselkoe@rics.bwh.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22997326" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/diagnosis/etiology/*prevention & control/therapy ; Amyloid beta-Peptides/cerebrospinal fluid/genetics/metabolism ; Animals ; Apolipoproteins E/genetics ; Biomarkers/analysis/cerebrospinal fluid ; Clinical Trials as Topic ; Disease Progression ; Genetic Predisposition to Disease ; Humans ; Life Style ; Mutation ; Peptide Fragments/cerebrospinal fluid ; Secondary Prevention
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Avian influenza. Surprising twist in debate over lab-made H5N1 (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, Jon -- New York, N.Y. -- Science. 2012 Mar 9;335(6073):1155-6. doi: 10.1126/science.335.6073.1155.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22403358" target="_blank"〉PubMed〈/a〉
    Keywords: Access to Information ; Animals ; Containment of Biohazards ; Disease Models, Animal ; Ferrets ; Humans ; Influenza A Virus, H5N1 Subtype/genetics/*pathogenicity ; Influenza, Human/epidemiology/transmission/*virology ; Mutation ; Orthomyxoviridae Infections/transmission/*virology ; Pandemics ; Publishing
    Print ISSN: 0036-8075
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    Avian influenza. The limits of avian flu studies in ferrets (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-02-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, Jon -- New York, N.Y. -- Science. 2012 Feb 3;335(6068):512-3. doi: 10.1126/science.335.6068.512.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22301288" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chickens ; *Disease Models, Animal ; *Ferrets ; Humans ; Influenza A Virus, H1N1 Subtype/pathogenicity ; Influenza A Virus, H5N1 Subtype/genetics/*pathogenicity ; Influenza in Birds/epidemiology ; Influenza, Human/epidemiology/transmission/*virology ; Mutation ; Orthomyxoviridae Infections/transmission/*virology ; Species Specificity
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    Avian influenza. On second thought, flu papers get go-ahead (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-04-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, Jon -- Malakoff, David -- New York, N.Y. -- Science. 2012 Apr 6;336(6077):19-20. doi: 10.1126/science.336.6077.19.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22491833" target="_blank"〉PubMed〈/a〉
    Keywords: *Access to Information ; Advisory Committees ; Animals ; Birds ; Humans ; Influenza A Virus, H5N1 Subtype/genetics/*pathogenicity ; Influenza in Birds/transmission/*virology ; Influenza, Human/transmission/virology ; Mammals ; Mutation ; National Institutes of Health (U.S.) ; Netherlands ; Orthomyxoviridae Infections/*virology ; Public Policy ; *Publishing ; United States
    Print ISSN: 0036-8075
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    Public health and biosecurity. Life sciences at a crossroads: respiratory transmissible H5N1 (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-01-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Osterholm, Michael T -- Henderson, Donald A -- New York, N.Y. -- Science. 2012 Feb 17;335(6070):801-2. doi: 10.1126/science.1218612. Epub 2012 Jan 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Infectious Disease Research and Division of Environmental Health Sciences, Medical School, University of Minnesota, Minneapolis, MN 55455, USA. mto@umn.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22267584" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Birds ; *Containment of Biohazards ; Humans ; Influenza A Virus, H5N1 Subtype/genetics/*pathogenicity ; Influenza Vaccines ; Influenza in Birds/epidemiology/transmission ; Influenza, Human/prevention & control/*transmission/virology ; *Information Dissemination/ethics ; Mutation ; Pandemics ; Public Health ; Publishing/ethics ; *Security Measures
    Print ISSN: 0036-8075
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    FKF1 conveys timing information for CONSTANS stabilization in photoperiodic flowering (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-05-26
    Description: Plants use day-length information to coordinate flowering time with the appropriate season to maximize reproduction. In Arabidopsis, the long day-specific expression of CONSTANS (CO) protein is crucial for flowering induction. Although light signaling regulates CO protein stability, the mechanism by which CO is stabilized in the long-day afternoon has remained elusive. Here, we demonstrate that FLAVIN-BINDING, KELCH REPEAT, F-BOX 1 (FKF1) protein stabilizes CO protein in the afternoon in long days. FKF1 interacts with CO through its LOV domain, and blue light enhances this interaction. In addition, FKF1 simultaneously removes CYCLING DOF FACTOR 1 (CDF1), which represses CO and FLOWERING LOCUS T (FT) transcription. Together with CO transcriptional regulation, FKF1 protein controls robust FT mRNA induction through multiple feedforward mechanisms that accurately control flowering timing.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3737243/" 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/PMC3737243/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Song, Young Hun -- Smith, Robert W -- To, Benjamin J -- Millar, Andrew J -- Imaizumi, Takato -- BB/F005237/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/F59011/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/G019621/Biotechnology and Biological Sciences Research Council/United Kingdom -- GM079712/GM/NIGMS NIH HHS/ -- R01 GM079712/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2012 May 25;336(6084):1045-9. doi: 10.1126/science.1219644.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of Washington, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22628657" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/genetics/growth & development/metabolism/*physiology ; Arabidopsis Proteins/chemistry/*genetics/*metabolism ; DNA-Binding Proteins/genetics/*metabolism ; Flowers/*growth & development ; Gene Expression Regulation, Plant ; Light ; Models, Biological ; Mutation ; *Photoperiod ; Plants, Genetically Modified ; Promoter Regions, Genetic ; Protein Binding ; Protein Interaction Domains and Motifs ; Protein Stability ; RNA, Messenger/genetics/metabolism ; RNA, Plant/genetics/metabolism ; Repressor Proteins/metabolism ; Transcription Factors/genetics/*metabolism ; Transcription, Genetic
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    Function and molecular mechanism of acetylation in autophagy regulation (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-04-28
    Description: Protein acetylation emerged as a key regulatory mechanism for many cellular processes. We used genetic analysis of Saccharomyces cerevisiae to identify Esa1 as a histone acetyltransferase required for autophagy. We further identified the autophagy signaling component Atg3 as a substrate for Esa1. Specifically, acetylation of K19 and K48 of Atg3 regulated autophagy by controlling Atg3 and Atg8 interaction and lipidation of Atg8. Starvation induced transient K19-K48 acetylation through spatial and temporal regulation of the localization of acetylase Esa1 and the deacetylase Rpd3 on pre-autophagosomal structures (PASs) and their interaction with Atg3. Attenuation of K19-K48 acetylation was associated with attenuation of autophagy. Increased K19-K48 acetylation after deletion of the deacetylase Rpd3 caused increased autophagy. Thus, protein acetylation contributes to control of autophagy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yi, Cong -- Ma, Meisheng -- Ran, Leili -- Zheng, Jingxiang -- Tong, Jingjing -- Zhu, Jing -- Ma, Chengying -- Sun, Yufen -- Zhang, Shaojin -- Feng, Wenzhi -- Zhu, Liyuan -- Le, Yan -- Gong, Xingqi -- Yan, Xianghua -- Hong, Bing -- Jiang, Fen-Jun -- Xie, Zhiping -- Miao, Di -- Deng, Haiteng -- Yu, Li -- New York, N.Y. -- Science. 2012 Apr 27;336(6080):474-7. doi: 10.1126/science.1216990.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉State Key Laboratory of Biomembrane and Membrane Biotechnology, School of Life Sciences, Tsinghua University, Beijing, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22539722" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; *Autophagy ; Carbohydrate Epimerases/genetics/metabolism ; Histone Acetyltransferases/genetics/*metabolism ; Histone Deacetylases/genetics/metabolism ; Microtubule-Associated Proteins/metabolism ; Mutation ; Phagosomes/metabolism ; Protein Processing, Post-Translational ; Recombinant Fusion Proteins/metabolism ; Saccharomyces cerevisiae/enzymology/genetics/*physiology ; Saccharomyces cerevisiae Proteins/chemistry/genetics/*metabolism ; Ubiquitin-Conjugating Enzymes/chemistry/genetics/*metabolism
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    FANCM limits meiotic crossovers (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-06-23
    Description: The number of meiotic crossovers (COs) is tightly regulated within a narrow range, despite a large excess of molecular precursors. The factors that limit COs remain largely unknown. Here, using a genetic screen in Arabidopsis thaliana, we identified the highly conserved FANCM helicase, which is required for genome stability in humans and yeasts, as a major factor limiting meiotic CO formation. The fancm mutant has a threefold-increased CO frequency as compared to the wild type. These extra COs arise not from the pathway that accounts for most of the COs in wild type, but from an alternate, normally minor pathway. Thus, FANCM is a key factor imposing an upper limit on the number of meiotic COs, and its manipulation holds much promise for plant breeding.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Crismani, Wayne -- Girard, Chloe -- Froger, Nicole -- Pradillo, Monica -- Santos, Juan Luis -- Chelysheva, Liudmila -- Copenhaver, Gregory P -- Horlow, Christine -- Mercier, Raphael -- New York, N.Y. -- Science. 2012 Jun 22;336(6088):1588-90. doi: 10.1126/science.1220381.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut National de la Recherche Agronomique (INRA), UMR1318, Institut Jean-Pierre Bourgin, Versailles, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22723424" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/*genetics/growth & development/physiology ; Arabidopsis Proteins/genetics/*metabolism ; Cation Transport Proteins/genetics/metabolism ; Chromosome Segregation ; Chromosomes, Plant/physiology/ultrastructure ; *Crossing Over, Genetic ; DNA Helicases/genetics/*metabolism ; Endonucleases/genetics/metabolism ; Genetic Complementation Test ; Homologous Recombination ; In Situ Hybridization, Fluorescence ; *Meiosis ; Mutation
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    Cilia at the node of mouse embryos sense fluid flow for left-right determination via Pkd2 (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-09-18
    Description: Unidirectional fluid flow plays an essential role in the breaking of left-right (L-R) symmetry in mouse embryos, but it has remained unclear how the flow is sensed by the embryo. We report that the Ca(2+) channel Polycystin-2 (Pkd2) is required specifically in the perinodal crown cells for sensing the nodal flow. Examination of mutant forms of Pkd2 shows that the ciliary localization of Pkd2 is essential for correct L-R patterning. Whereas Kif3a mutant embryos, which lack all cilia, failed to respond to an artificial flow, restoration of primary cilia in crown cells rescued the response to the flow. Our results thus suggest that nodal flow is sensed in a manner dependent on Pkd2 by the cilia of crown cells located at the edge of the node.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3711115/" 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/PMC3711115/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yoshiba, Satoko -- Shiratori, Hidetaka -- Kuo, Ivana Y -- Kawasumi, Aiko -- Shinohara, Kyosuke -- Nonaka, Shigenori -- Asai, Yasuko -- Sasaki, Genta -- Belo, Jose Antonio -- Sasaki, Hiroshi -- Nakai, Junichi -- Dworniczak, Bernd -- Ehrlich, Barbara E -- Pennekamp, Petra -- Hamada, Hiroshi -- P30 DK090744/DK/NIDDK NIH HHS/ -- P50 DK057328/DK/NIDDK NIH HHS/ -- R01 DK087844/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2012 Oct 12;338(6104):226-31. doi: 10.1126/science.1222538. Epub 2012 Sep 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Developmental Genetics Group, Graduate School of Frontier Biosciences, Osaka University, 1-3 Yamada-oka, Suita, 565-0871 Osaka, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22983710" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Body Fluids/physiology ; *Body Patterning ; Calcium/metabolism ; Cilia/metabolism/physiology ; Embryo, Mammalian/anatomy & histology/cytology/*physiology ; Gene Expression Regulation, Developmental ; Intercellular Signaling Peptides and Proteins/metabolism ; Kinesin/genetics ; Left-Right Determination Factors/genetics/*metabolism ; Mice ; Mice, Mutant Strains ; Mutation ; Organizers, Embryonic/cytology/*physiology ; Signal Transduction ; TRPP Cation Channels/genetics/*metabolism
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    The biology of genomes. HDL itself does not prevent heart attacks (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-05-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, Elizabeth -- New York, N.Y. -- Science. 2012 May 25;336(6084):977. doi: 10.1126/science.336.6084.977.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22628634" target="_blank"〉PubMed〈/a〉
    Keywords: Humans ; Lipase/genetics ; Lipoproteins, HDL/blood/*physiology ; Lipoproteins, LDL/blood ; Mutation ; Myocardial Infarction/epidemiology/*genetics/*prevention & control
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    Computational design of self-assembling protein nanomaterials with atomic level accuracy (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-06-02
    Description: We describe a general computational method for designing proteins that self-assemble to a desired symmetric architecture. Protein building blocks are docked together symmetrically to identify complementary packing arrangements, and low-energy protein-protein interfaces are then designed between the building blocks in order to drive self-assembly. We used trimeric protein building blocks to design a 24-subunit, 13-nm diameter complex with octahedral symmetry and a 12-subunit, 11-nm diameter complex with tetrahedral symmetry. The designed proteins assembled to the desired oligomeric states in solution, and the crystal structures of the complexes revealed that the resulting materials closely match the design models. The method can be used to design a wide variety of self-assembling protein nanomaterials.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4138882/" 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/PMC4138882/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉King, Neil P -- Sheffler, William -- Sawaya, Michael R -- Vollmar, Breanna S -- Sumida, John P -- Andre, Ingemar -- Gonen, Tamir -- Yeates, Todd O -- Baker, David -- RR-15301/RR/NCRR NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Jun 1;336(6085):1171-4. doi: 10.1126/science.1219364.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Washington, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22654060" target="_blank"〉PubMed〈/a〉
    Keywords: Chromatography, Gel ; Cloning, Molecular ; Computational Biology ; Computer Simulation ; Crystallography, X-Ray ; Escherichia coli/genetics/metabolism ; Hydrogen Bonding ; Microscopy, Electron ; Models, Molecular ; Molecular Weight ; Mutation ; *Nanostructures ; *Protein Engineering ; *Protein Multimerization ; Protein Structure, Secondary ; Protein Subunits/*chemistry/genetics ; Proteins/*chemistry/genetics
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    Septin-mediated plant cell invasion by the rice blast fungus, Magnaporthe oryzae (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-06-23
    Description: To cause rice blast disease, the fungus Magnaporthe oryzae develops a pressurized dome-shaped cell called an appressorium, which physically ruptures the leaf cuticle to gain entry to plant tissue. Here, we report that a toroidal F-actin network assembles in the appressorium by means of four septin guanosine triphosphatases, which polymerize into a dynamic, hetero-oligomeric ring. Septins scaffold F-actin, via the ezrin-radixin-moesin protein Tea1, and phosphatidylinositide interactions at the appressorium plasma membrane. The septin ring assembles in a Cdc42- and Chm1-dependent manner and forms a diffusion barrier to localize the inverse-bin-amphiphysin-RVS-domain protein Rvs167 and the Wiskott-Aldrich syndrome protein Las17 at the point of penetration. Septins thereby provide the cortical rigidity and membrane curvature necessary for protrusion of a rigid penetration peg to breach the leaf surface.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dagdas, Yasin F -- Yoshino, Kae -- Dagdas, Gulay -- Ryder, Lauren S -- Bielska, Ewa -- Steinberg, Gero -- Talbot, Nicholas J -- Biotechnology and Biological Sciences Research Council/United Kingdom -- New York, N.Y. -- Science. 2012 Jun 22;336(6088):1590-5. doi: 10.1126/science.1222934.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Biosciences, University of Exeter, Exeter, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22723425" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/*physiology/ultrastructure ; Actins/*metabolism ; Cell Membrane/metabolism/ultrastructure ; Diffusion ; Fungal Proteins/chemistry/genetics/*metabolism ; Magnaporthe/genetics/*pathogenicity/physiology/ultrastructure ; Microfilament Proteins/metabolism ; Mutation ; Oryza/*microbiology ; Phosphatidylinositols/metabolism ; Plant Diseases/*microbiology ; Plant Leaves/microbiology ; Protein Interaction Domains and Motifs ; Recombinant Fusion Proteins/metabolism ; Septins/*chemistry/genetics/*metabolism ; cdc42 GTP-Binding Protein/metabolism
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    Medicine. Drug trial offers uncertain start in race to save children with progeria (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-09-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Couzin-Frankel, Jennifer -- New York, N.Y. -- Science. 2012 Sep 28;337(6102):1594-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23019622" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Child, Preschool ; Clinical Trials as Topic/*economics/*statistics & numerical data ; Enzyme Inhibitors/*therapeutic use ; Farnesyltranstransferase/antagonists & inhibitors ; Foundations/organization & administration ; Humans ; Lamin Type A/genetics ; Mice ; Mutation ; Patient Selection ; Piperidines/*therapeutic use ; Progeria/*drug therapy/economics/*genetics ; Pyridines/*therapeutic use ; Uncertainty ; United States ; United States Public Health Service
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    A single promoter inversion switches Photorhabdus between pathogenic and mutualistic states (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-07-07
    Description: Microbial populations stochastically generate variants with strikingly different properties, such as virulence or avirulence and antibiotic tolerance or sensitivity. Photorhabdus luminescens bacteria have a variable life history in which they alternate between pathogens to a wide variety of insects and mutualists to their specific host nematodes. Here, we show that the P. luminescens pathogenic variant (P form) switches to a smaller-cell variant (M form) to initiate mutualism in host nematode intestines. A stochastic promoter inversion causes the switch between the two distinct forms. M-form cells are much smaller (one-seventh the volume), slower growing, and less bioluminescent than P-form cells; they are also avirulent and produce fewer secondary metabolites. Observations of form switching by individual cells in nematodes revealed that the M form persisted in maternal nematode intestines, were the first cells to colonize infective juvenile (IJ) offspring, and then switched to P form in the IJ intestine, which armed these nematodes for the next cycle of insect infection.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4006969/" 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/PMC4006969/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Somvanshi, Vishal S -- Sloup, Rudolph E -- Crawford, Jason M -- Martin, Alexander R -- Heidt, Anthony J -- Kim, Kwi-suk -- Clardy, Jon -- Ciche, Todd A -- 1K99 GM097096-01/GM/NIGMS NIH HHS/ -- K99 GM097096/GM/NIGMS NIH HHS/ -- R00 GM097096/GM/NIGMS NIH HHS/ -- R01 GM086258/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2012 Jul 6;337(6090):88-93. doi: 10.1126/science.1216641.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Molecular Genetics, Michigan State University, East Lansing, MI 48824, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22767929" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Fimbriae Proteins/genetics ; Gene Expression Regulation, Bacterial ; Genome, Bacterial ; Intestines/microbiology ; Moths/*microbiology ; Mutation ; Phenotype ; Photorhabdus/cytology/*genetics/growth & development/*pathogenicity ; *Promoter Regions, Genetic ; Rhabditoidea/*microbiology ; *Sequence Inversion ; *Symbiosis ; Virulence/genetics
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    Oscillatory dynamics of Cdc42 GTPase in the control of polarized growth (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-05-19
    Description: Cells promote polarized growth by activation of Rho-family protein Cdc42 at the cell membrane. We combined experiments and modeling to study bipolar growth initiation in fission yeast. Concentrations of a fluorescent marker for active Cdc42, Cdc42 protein, Cdc42-activator Scd1, and scaffold protein Scd2 exhibited anticorrelated fluctuations and oscillations with a 5-minute average period at polarized cell tips. These dynamics indicate competition for active Cdc42 or its regulators and the presence of positive and delayed negative feedbacks. Cdc42 oscillations and spatial distribution were sensitive to the amounts of Cdc42-activator Gef1 and to the activity of Cdc42-dependent kinase Pak1, a negative regulator. Feedbacks regulating Cdc42 oscillations and spatial self-organization appear to provide a flexible mechanism for fission yeast cells to explore polarization states and to control their morphology.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3681419/" 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/PMC3681419/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Das, Maitreyi -- Drake, Tyler -- Wiley, David J -- Buchwald, Peter -- Vavylonis, Dimitrios -- Verde, Fulvia -- 1R01GM095867/GM/NIGMS NIH HHS/ -- R01 GM095867/GM/NIGMS NIH HHS/ -- R21 GM083928/GM/NIGMS NIH HHS/ -- R21GM083928/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2012 Jul 13;337(6091):239-43. doi: 10.1126/science.1218377. Epub 2012 May 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Pharmacology (R-189), University of Miami Miller School of Medicine, Post Office Box 016189, Miami, FL 33101, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22604726" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Cycle Proteins/metabolism ; Guanine Nucleotide Exchange Factors/metabolism ; Microscopy, Fluorescence ; Models, Biological ; Mutation ; Recombinant Fusion Proteins/metabolism ; Schizosaccharomyces/cytology/*enzymology/genetics/*growth & development ; Schizosaccharomyces pombe Proteins/*metabolism ; cdc42 GTP-Binding Protein/*metabolism ; p21-Activated Kinases/metabolism
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    Growing microtubules push the oocyte nucleus to polarize the Drosophila dorsal-ventral axis (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-04-14
    Description: The Drosophila dorsal-ventral (DV) axis is polarized when the oocyte nucleus migrates from the posterior to the anterior margin of the oocyte. Prior work suggested that dynein pulls the nucleus to the anterior side along a polarized microtubule cytoskeleton, but this mechanism has not been tested. By imaging live oocytes, we find that the nucleus migrates with a posterior indentation that correlates with its direction of movement. Furthermore, both nuclear movement and the indentation depend on microtubule polymerization from centrosomes behind the nucleus. Thus, the nucleus is not pulled to the anterior but is pushed by the force exerted by growing microtubules. Nuclear migration and DV axis formation therefore depend on centrosome positioning early in oogenesis and are independent of anterior-posterior axis formation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3459055/" 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/PMC3459055/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhao, Tongtong -- Graham, Owen S -- Raposo, Alexandre -- St Johnston, Daniel -- 080007/Wellcome Trust/United Kingdom -- 092096/Wellcome Trust/United Kingdom -- A14492/Cancer Research UK/United Kingdom -- Cancer Research UK/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2012 May 25;336(6084):999-1003. doi: 10.1126/science.1219147. Epub 2012 Apr 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Gurdon Institute and the Department of Genetics, University of Cambridge, Cambridge, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22499806" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Body Patterning ; Cell Nucleus/*physiology/ultrastructure ; Cell Polarity ; Centrosome/physiology ; Drosophila ; Drosophila Proteins/physiology ; Dyneins/physiology ; Microtubule-Organizing Center/physiology/ultrastructure ; Microtubules/*physiology/ultrastructure ; Movement ; Mutation ; Nuclear Envelope/physiology/ultrastructure ; Oocytes/*physiology/ultrastructure ; *Oogenesis
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    Regulation of a hybrid gene by glucose and temperature in hamster fibroblasts (1984)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1984-10-12
    Description: A novel eukaryotic hybrid gene has been constructed from the 5' sequence of a rat gene and the bacterial neomycin-resistance gene. After transfection into hamster fibroblasts, the neo transcripts can be induced to high levels by the absence of glucose. Furthermore, this hybrid gene can be regulated by temperature when it is introduced into a temperature-sensitive mutant cell line.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Attenello, J W -- Lee, A S -- CA-27607/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1984 Oct 12;226(4671):187-90.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6484570" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cricetinae ; DNA, Recombinant ; Drug Resistance, Microbial ; Fibroblasts ; *Gene Expression Regulation ; Genes, Bacterial ; *Genes, Regulator ; Glucose/*pharmacology ; *HSP70 Heat-Shock Proteins ; Membrane Proteins/biosynthesis/*genetics ; Mutation ; Neomycin/pharmacology ; Rats ; Temperature ; Transcription, Genetic ; Transfection
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    Reversal of knob formation on Plasmodium falciparum-infected erythrocytes (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-10-05
    Description: The human malarial parasite Plasmodium falciparum can produce surface protrusions (knobs) on infected erythrocytes; however, long-term culturing of the parasite results in the appearance of knobless cells. In this study it was found that a knob-producing clone lost the ability to produce knobs in vitro. Furthermore, a clone not producing knobs derived from the knob-producing clone regained the capacity to produce knobby cells in vitro. Certain parasite proteins were associated with the knobby phenotype but not with the knobless type. These results indicate that the parasites change in vitro in a spontaneous and reversible manner independent of immunological selection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gritzmacher, C A -- Reese, R T -- AI 18695/AI/NIAID NIH HHS/ -- DRR 00833/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1984 Oct 5;226(4670):65-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6382613" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Clone Cells ; Erythrocytes/*parasitology/ultrastructure ; Humans ; Mutation ; Phenotype ; Plasmodium falciparum/analysis/genetics/growth & development/*physiology ; Proteins/analysis
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  • 83
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    Time-varying magnetic fields: effect on DNA synthesis (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-02-24
    Description: Human fibroblasts have exhibited enhanced DNA synthesis when exposed to sinusoidally varying magnetic fields for a wide range of frequencies (15 hertz to 4 kilohertz) and amplitudes (2.3 X 10(-6) to 5.6 X 10(-4) tesla). This effect, which is at maximum during the middle of the S phase of the cell cycle, appears to be independent of the time derivative of the magnetic field, suggesting an underlying mechanism other than Faraday's law. The threshold is estimated to be between 0.5 X 10(-5) and 2.5 X 10(-5) tesla per second. These results bring into question the allegedly specific magnetic wave shapes now used in therapeutic devices for bone nonunion. The range of magnetic field amplitudes tested encompass the geomagnetic field, suggesting the possibility of mutagenic interactions directly arising from short-term changes in the earth's field.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liboff, A R -- Williams, T Jr -- Strong, D M -- Wistar, R Jr -- New York, N.Y. -- Science. 1984 Feb 24;223(4638):818-20.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6695183" target="_blank"〉PubMed〈/a〉
    Keywords: Cells, Cultured ; DNA/*biosynthesis ; Humans ; *Magnetics ; Mutation ; Periodicity
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  • 84
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    Transfection of the DNA polymerase-alpha gene (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-11-16
    Description: DNA polymerase-alpha is the major replicative DNA polymerase in animal cells. The gene coding for a mutant DNA polymerase-alpha was transferred from one cell to another by transfection of DNA from mutant cells. The DNA was isolated from a mutant hamster cell line resistant to aphidicolin, a specific inhibitor of DNA polymerase-alpha, and transferred into an aphidicolin-sensitive cell line. The resulting transfectants exhibited increased survival in the presence of aphidicolin and contained an aphidicolin-resistant DNA polymerase-alpha.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, P K -- Loeb, L A -- CA07418/CA/NCI NIH HHS/ -- CA24845/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1984 Nov 16;226(4676):833-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6436977" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aphidicolin ; Cell Line ; Clone Cells ; Cricetinae ; Cricetulus/genetics ; DNA Polymerase II/*genetics ; Diterpenes/pharmacology ; Escherichia coli/genetics ; Humans ; Mice ; Mutation ; Salmon/genetics ; *Transfection
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  • 85
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    Homologous recombination catalyzed by mammalian cell extracts in vitro (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-12-07
    Description: An assay was developed to detect recombination events taking place in an in vitro reaction. Extracts of cultured mouse preB lymphocytes were found to catalyze homologous recombination between substrate DNA molecules but not site-specific recombination between cloned mouse immunoglobulin D and J genes. Addition of deoxyribonucleoside triphosphates increased the frequency of homologous recombination. This recombination activity was not observed in two differentiated lymphocyte cell lines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Darby, V -- Blattner, F -- AI19325/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1984 Dec 7;226(4679):1213-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6334360" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes ; Cells, Cultured ; Crossing Over, Genetic ; DNA, Viral ; Immunoglobulin Variable Region/genetics ; Mice ; Mutation ; Nucleoproteins/genetics ; *Recombination, Genetic
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  • 86
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    A trans-acting product needed for P factor transposition in Drosophila (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-12-07
    Description: A transposable genetic element of the P family in Drosophila melanogaster was found to be unstable in the presence of other P elements but stable in their absence. A sensitive assay for P transpositional activity is provided by the snw allele, a defective P insert in the singed bristle locus which becomes hypermutable only in the presence of complete elements. This measure of activity was highly correlated with a type of female sterility normally associated with P activity. There was no cross-reactivity with transposase from another hybrid dysgenesis-causing element (the I factor).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Engels, W R -- GM30948/GM/NIGMS NIH HHS/ -- PCM8104332/PC/NCI NIH HHS/ -- New York, N.Y. -- Science. 1984 Dec 7;226(4679):1194-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6095450" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cross Reactions ; *DNA Transposable Elements ; Drosophila melanogaster/*genetics ; Female ; Gonadal Dysgenesis/genetics ; Infertility, Female/genetics ; Male ; Mutation
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  • 87
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    Activation of a c-K-ras oncogene by somatic mutation in mouse lymphomas induced by gamma radiation (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-09-14
    Description: Mouse tumors induced by gamma radiation are a useful model system for oncogenesis. DNA from such tumors contains an activated K-ras oncogene that can transform NIH 3T3 cells. This report describes the cloning of a fragment of the mouse K-ras oncogene containing the first exon from both a transformant in rat-2 cells and the brain of the same mouse that developed the tumor. Hybrid constructs containing one of the two pieces were made and only the plasmid including the first exon from the transformant gave rise to foci in NIH 3T3 cells. There was only a single base difference (G----A) in the exonic sequence, which changed glycine to aspartic acid in the transformant. By use of a synthetic oligonucleotide the presence of the mutation was demonstrated in the original tumor, ruling out modifications during DNA-mediated gene transfer and indicating that the alteration was present in the thymic lymphoma but absent from other nonmalignant tissue. The results are compatible with gamma radiation being a source of point mutations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guerrero, I -- Villasante, A -- Corces, V -- Pellicer, A -- CA-36327/CA/NCI NIH HHS/ -- GM-32036/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1984 Sep 14;225(4667):1159-62.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6474169" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Transformation, Neoplastic ; Cells, Cultured ; Cloning, Molecular ; Gamma Rays ; Lymphoma/*genetics ; Mice ; Mutation ; Neoplasms, Radiation-Induced/*genetics ; Nucleic Acid Hybridization ; *Oncogenes ; Rats
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  • 88
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    DNA markers for nervous system diseases (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-09-21
    Description: Recombinant DNA technology has provided a vast new source of DNA markers displaying heritable sequence variation in humans. These markers can be used in family studies to identify the chromosomal location of defective genes causing nervous system disorders. The discovery of a DNA marker linked to Huntington's disease has opened new avenues of research into this disorder and may ultimately permit cloning and characterization of the defective gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gusella, J F -- Tanzi, R E -- Anderson, M A -- Hobbs, W -- Gibbons, K -- Raschtchian, R -- Gilliam, T C -- Wallace, M R -- Wexler, N S -- Conneally, P M -- NS16367/NS/NINDS NIH HHS/ -- NS20012/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1984 Sep 21;225(4668):1320-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6089346" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Base Sequence ; Chromosome Mapping ; Cloning, Molecular ; DNA/*genetics ; DNA Restriction Enzymes ; *DNA, Recombinant ; Female ; *Genes ; *Genetic Linkage ; *Genetic Markers ; Genetic Vectors ; Humans ; Huntington Disease/*genetics ; Male ; Mutation ; Pedigree ; Phenotype ; Polymorphism, Genetic
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  • 89
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    Requirement for a signal sequence in biological expression of the v-sis oncogene (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-12-07
    Description: The protein encoded by the simian sarcoma virus oncogene (v-sis) contains a signal sequence, derived from the envelope gene of the parental retrovirus, which is required for transformation. Removal of the proposed signal sequence was correlated with loss of biological activity. This activity was restored to inactive deletion mutants by fusion with the coding region for a heterologous signal sequence. Biological activity of v-sis was also abolished by either a small deletion within the coding region of the signal sequence or by a point mutation introduced by site-directed mutagenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hannink, M -- Donoghue, D J -- CA34456/CA/NCI NIH HHS/ -- GM07313/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1984 Dec 7;226(4679):1197-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6095451" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Transformation, Viral ; *Gene Expression Regulation ; Mutation ; *Oncogenes ; *Protein Biosynthesis ; Retroviridae/*genetics ; Sarcoma Virus, Woolly Monkey/*genetics ; Viral Proteins/biosynthesis
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  • 90
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    The continuing tale of a small worm (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-07-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lewin, R -- New York, N.Y. -- Science. 1984 Jul 13;225(4658):153-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6729473" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis/*anatomy & histology/genetics/growth & development ; Mutation ; Nervous System/anatomy & histology/growth & development
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  • 91
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    Caenorhabditis elegans: getting to know you (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-07-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1984 Jul 6;225(4657):40-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6729468" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis/genetics/*growth & development ; Cell Differentiation ; Cell Survival ; Female ; Male ; Mutation
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  • 92
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    Need a catalyst? Design an enzyme (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-01-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maugh, T H 2nd -- New York, N.Y. -- Science. 1984 Jan 20;223(4633):269-71.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6608147" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Binding Sites ; Biochemistry/*methods ; Catalysis ; *Cloning, Molecular ; Enzymes/genetics/*metabolism ; Mutation ; Structure-Activity Relationship ; Substrate Specificity ; Tetrahydrofolate Dehydrogenase/metabolism ; Tyrosine-tRNA Ligase/metabolism ; beta-Lactamases/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 93
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    The significance of responses of the genome to challenge (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-11-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McClintock, B -- New York, N.Y. -- Science. 1984 Nov 16;226(4676):792-801.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15739260" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Nucleus/metabolism ; Chromosome Breakage ; Chromosomes, Plant/physiology/radiation effects ; *DNA Transposable Elements ; Gene Expression Regulation ; *Gene Expression Regulation, Plant ; Genetics/history ; *Genome, Plant ; History, 20th Century ; Hybridization, Genetic ; Meiosis ; Mitosis ; Mutation ; Plant Viruses/physiology ; Telophase ; Zea mays/*genetics/physiology/virology
    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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  • 94
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    Retinoblastoma: clues to human oncogenesis (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-03-09
    Description: The retinoblastoma gene can be considered a model for a class of recessive human cancer genes that have a "suppressor" or "regulatory" function. The loss or inactivation of both alleles of this gene appears to be a primary mechanism in the development of retinoblastoma. Such a mechanism is in direct contrast to that of putative human oncogenes which are thought to induce tumorigenesis following activation or alteration. The high incidence of second primary tumors among patients who inherit one inactive retinoblastoma allele also suggests that this cancer gene plays a key role in the etiology of several other primary malignancies. Finally, the observation that extra nonrandom copies of specific chromosomal regions occur in some of these tumors provides circumstantial evidence that an "expressor" gene (possibly an oncogene) may be involved in retinoblastoma development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Murphree, A L -- Benedict, W F -- EY-02715/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1984 Mar 9;223(4640):1028-33.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6320372" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/genetics ; Alleles ; Child ; Chromosome Deletion ; Chromosome Mapping ; Chromosomes, Human, 13-15 ; Chromosomes, Human, 6-12 and X ; Eye Neoplasms/*genetics ; Genes, Recessive ; Genotype ; Humans ; Kidney Neoplasms/genetics ; Mutation ; Neuroblastoma/genetics ; *Oncogenes ; Polymorphism, Genetic ; Retinoblastoma/*genetics ; *Suppression, Genetic ; Translocation, Genetic ; Wilms Tumor/genetics
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  • 95
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    Evolution of proteolytic enzymes (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-04-27
    Description: Proteolytic enzymes have many physiological functions, ranging from generalized protein digestion to more specific regulated processes such as the activation of zymogens, blood coagulation and the lysis of fibrin clots, the release of hormones and pharmacologically active peptides from precursor proteins, and the transport of secretory proteins across membranes. They are present in all forms of living organisms. Comparisons of amino acid sequences, three-dimensional structures, and enzymatic reaction mechanisms of proteases indicate that there are distinct families of these proteins. Changes in molecular structure and function have accompanied the evolution of proteolytic enzymes and their inhibitors, each having relatively simple roles in primitive organisms and more diverse and more complex functions in higher organisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Neurath, H -- GM-15731/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1984 Apr 27;224(4647):350-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6369538" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Binding Sites ; *Biological Evolution ; Blood Coagulation ; Chemistry, Physical ; Enzyme Activation ; Enzyme Precursors/metabolism ; Genes ; Humans ; Mutation ; *Peptide Hydrolases/analysis/genetics/metabolism ; Peptides/metabolism ; Physicochemical Phenomena ; Protease Inhibitors/analysis/metabolism ; Protein Conformation ; Protein Sorting Signals ; Substrate Specificity
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  • 96
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    Sindbis virus mutants selected for rapid growth in cell culture display attenuated virulence in animals (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-07-27
    Description: Mutants of Sindbis virus were selected for rapid growth in baby hamster kidney (BHK) cell cultures and screened for attenuation of virulence in suckling mice. Comparisons among independently isolated virulent and attenuated strains, as well as a classical reversion analysis, showed that accelerated penetration of BHK cells was correlated with attenuation in vivo. Both phenotypic changes resulted from a reorganization of virion structure as detected by monoclonal antibodies. These results suggest that mutants selected for rapid growth in cell culture may be useful as attenuated vaccines and for studies of the molecular basis of virus pathogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Olmsted, R A -- Baric, R S -- Sawyer, B A -- Johnston, R E -- AI19433/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1984 Jul 27;225(4660):424-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6204381" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/immunology ; Antibodies, Viral/immunology ; Cells, Cultured ; Cricetinae ; Kidney/cytology ; Mice ; Mutation ; Neutralization Tests ; RNA/biosynthesis ; Sindbis Virus/genetics/growth & development/immunology/*pathogenicity ; Togaviridae Infections/microbiology
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  • 97
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    Expression of cellular oncogenes in human malignancies (1984)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1984-04-20
    Description: Cellular oncogenes have been implicated in the induction of malignant transformation in some model systems in vitro and may be related to malignancies in vivo in some vertebrate species. This article describes a study of the expression of 15 cellular oncogenes in fresh human tumors from 54 patients, representing 20 different tumor types. More than one cellular oncogene was transcriptionally active in all of the tumors examined. In 14 patients it was possible to study normal and malignant tissue from the same organ. In many of these patients, the transcriptional activity of certain oncogenes was greater in the malignant than the normal tissue. The cellular fes (feline sarcoma) oncogene, not previously known to be transcribed in mammalian tissue, was found to be active in lung and hematopoietic malignancies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Slamon, D J -- deKernion, J B -- Verma, I M -- Cline, M J -- AM 18058/AM/NIADDK NIH HHS/ -- CA 15619/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1984 Apr 20;224(4646):256-62.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6538699" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/genetics ; Breast Neoplasms/genetics ; Carcinogens/pharmacology ; Cell Differentiation ; Cell Division ; Cell Transformation, Neoplastic ; Female ; Gastrointestinal Neoplasms/genetics ; Gene Amplification ; Genes, Viral ; Genital Neoplasms, Female/genetics ; Humans ; Kidney Neoplasms/genetics ; Leukemia/genetics ; Lymphoma/genetics ; Methylation ; Mutation ; Neoplasms/*genetics ; Nucleic Acid Hybridization ; *Oncogenes ; RNA, Messenger/genetics ; RNA, Neoplasm/genetics ; Sarcoma/genetics ; *Transcription, Genetic ; Translocation, Genetic
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  • 98
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    Molecular dissection of transcriptional control elements within the long terminal repeat of the retrovirus (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-01-20
    Description: The retroviral long terminal repeat (LTR) contains transcriptional control elements that affect viral gene expression. By deletion mutagenesis of the genome of the cloned Abelson murine leukemia virus, regulatory signals could be mapped to at least three domains within the LTR. A defective 5' LTR that did not sustain transforming gene function was complemented by an intact LTR positioned at the 3' end of the genome. This versatility of the retroviral genome with respect to its transcriptional control elements appears to provide a strong selective advantage for viral gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Srinivasan, A -- Reddy, E P -- Dunn, C Y -- Aaronson, S A -- New York, N.Y. -- Science. 1984 Jan 20;223(4633):286-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6322296" target="_blank"〉PubMed〈/a〉
    Keywords: Abelson murine leukemia virus/*genetics ; Animals ; Cell Line ; Cell Transformation, Viral ; Cloning, Molecular ; *Gene Expression Regulation ; *Genes, Viral ; Leukemia Virus, Murine/*genetics ; Mice ; Mutation ; *Repetitive Sequences, Nucleic Acid ; *Transcription, Genetic ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Malignant activation of a K-ras oncogene in lung carcinoma but not in normal tissue of the same patient (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-02-17
    Description: A single genetic alteration, a guanine-to-cytosine transversion, is responsible for the acquisition of malignant properties by K-ras genes of two human tumor cell lines established from carcinomas of the bladder (A1698) and lung (A2182). As a consequence, arginine instead of the normal glycine is incorporated into the K-ras-coded p21 proteins at amino acid position 12. This mutation creates a restriction enzyme polymorphism that can be used to screen human cells for transforming K-ras genes. This approach was used to identify the mutational event responsible for the malignant activation of a K-ras oncogene in a squamous cell lung carcinoma of a 66-year-old man; this point mutation was not present in either the normal bronchial or parenchymal tissue or in the blood lymphocytes. Hence, malignant activation of a ras oncogene appears to be specifically associated with the development of a human neoplasm.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Santos, E -- Martin-Zanca, D -- Reddy, E P -- Pierotti, M A -- Della Porta, G -- Barbacid, M -- New York, N.Y. -- Science. 1984 Feb 17;223(4637):661-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6695174" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; *Cell Transformation, Neoplastic ; DNA, Neoplasm/genetics ; Genes, Dominant ; Humans ; Lung Neoplasms/*genetics ; Mutation ; *Oncogenes ; Organ Specificity ; Polymorphism, Genetic
    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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