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  • 1
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    Genetic definition and sequence analysis of Arabidopsis centromeres (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-01-05
    Description: High-precision genetic mapping was used to define the regions that contain centromere functions on each natural chromosome in Arabidopsis thaliana. These regions exhibited dramatic recombinational repression and contained complex DNA surrounding large arrays of 180-base pair repeats. Unexpectedly, the DNA within the centromeres was not merely structural but also encoded several expressed genes. The regions flanking the centromeres were densely populated by repetitive elements yet experienced normal levels of recombination. The genetically defined centromeres were well conserved among Arabidopsis ecotypes but displayed limited sequence homology between different chromosomes, excluding repetitive DNA. This investigation provides a platform for dissecting the role of individual sequences in centromeres in higher eukaryotes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Copenhaver, G P -- Nickel, K -- Kuromori, T -- Benito, M I -- Kaul, S -- Lin, X -- Bevan, M -- Murphy, G -- Harris, B -- Parnell, L D -- McCombie, W R -- Martienssen, R A -- Marra, M -- Preuss, D -- New York, N.Y. -- Science. 1999 Dec 24;286(5449):2468-74.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Chicago, Department of Molecular Genetics and Cell Biology, 1103 East 57 Street, Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10617454" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/chemistry/*genetics ; Base Composition ; Base Sequence ; Centromere/*genetics/physiology ; Conserved Sequence ; Contig Mapping ; Crosses, Genetic ; Crossing Over, Genetic ; DNA, Plant/chemistry/*genetics ; Gene Expression ; *Genes, Plant ; Meiosis ; Models, Genetic ; *Recombination, Genetic ; *Repetitive Sequences, Nucleic Acid ; Retroelements ; Sequence Analysis, DNA
    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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    Bacteriophytochromes: phytochrome-like photoreceptors from nonphotosynthetic eubacteria (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-01-05
    Description: Phytochromes are a family of photoreceptors used by green plants to entrain their development to the light environment. The distribution of these chromoproteins has been expanded beyond photoautotrophs with the discovery of phytochrome-like proteins in the nonphotosynthetic eubacteria Deinococcus radiodurans and Pseudomonas aeruginosa. Like plant phytochromes, the D. radiodurans receptor covalently binds linear tetrapyrroles autocatalytically to generate a photochromic holoprotein. However, the attachment site is distinct, using a histidine to potentially form a Schiff base linkage. Sequence homology and mutational analysis suggest that D. radiodurans bacteriophytochrome functions as a light-regulated histidine kinase, which helps protect the bacterium from visible light.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Davis, S J -- Vener, A V -- Vierstra, R D -- New York, N.Y. -- Science. 1999 Dec 24;286(5449):2517-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Genetics, Cellular and Molecular Biology Program and Department of Horticulture, University of Wisconsin-Madison, 1575 Linden Drive, Madison, WI 53706, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10617469" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acid Substitution ; Bacterial Proteins/chemistry/genetics/*metabolism ; Biliverdine/analogs & derivatives/metabolism ; Binding Sites ; Gram-Positive Cocci/genetics/*metabolism ; Histidine/metabolism ; Light ; Molecular Sequence Data ; Mutagenesis, Site-Directed ; Photoreceptors, Microbial/chemistry/genetics/*metabolism ; Phytochrome/metabolism ; Protein Kinases/chemistry/genetics/*metabolism ; Pseudomonas aeruginosa/*metabolism ; Signal Transduction
    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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  • 3
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    Role of the mouse ank gene in control of tissue calcification and arthritis (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-07-15
    Description: Mutation at the mouse progressive ankylosis (ank) locus causes a generalized, progressive form of arthritis accompanied by mineral deposition, formation of bony outgrowths, and joint destruction. Here, we show that the ank locus encodes a multipass transmembrane protein (ANK) that is expressed in joints and other tissues and controls pyrophosphate levels in cultured cells. A highly conserved gene is present in humans and other vertebrates. These results identify ANK-mediated control of pyrophosphate levels as a possible mechanism regulating tissue calcification and susceptibility to arthritis in higher animals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ho, A M -- Johnson, M D -- Kingsley, D M -- 5T32GM07365/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2000 Jul 14;289(5477):265-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology and Howard Hughes Medical Institute, Beckman Center B300, Stanford University School of Medicine, Stanford, CA 94305-5327, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10894769" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arthritis/*genetics/metabolism/pathology ; Base Sequence ; Biological Transport ; COS Cells ; Calcinosis/*genetics ; Chromosome Mapping ; Cloning, Molecular ; Dna ; Diphosphates/*metabolism ; Durapatite/metabolism ; Gene Expression ; Genetic Complementation Test ; Humans ; Membrane Proteins/*genetics/metabolism/*physiology ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; Mutation ; Phenotype ; Phosphate Transport Proteins ; Physical Chromosome Mapping ; Sequence Homology, Nucleic Acid ; Tissue Distribution
    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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    Molecular biology. The mad ways of meiosis (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-08-05
    Description: Reproductive cells that are destined to become sperm or egg undergo meiotic division during which the chromosome number is halved. As Sluder and McCollum explain in their Perspective, new findings (Shonn et al.) in yeast show that there is a spindle checkpoint that operates during meiosis to ensure that an equal number of replicated chromosomes arrives at each pole of the cell. One of the components of this meiotic spindle checkpoint turns out to be Mad2, which gives the signal to halt meiosis if it looks like unequal chromosome segregation is taking place.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sluder, G -- McCollum, D -- New York, N.Y. -- Science. 2000 Jul 14;289(5477):254-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, University of Massachusetts Medical School, Worcester, MA 01655, USA. greenfield.sluder@umassmed.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10917849" target="_blank"〉PubMed〈/a〉
    Keywords: Calcium-Binding Proteins/physiology ; *Carrier Proteins ; Cell Cycle Proteins ; Chromosome Aberrations ; Chromosome Disorders ; Chromosome Segregation ; Fungal Proteins/physiology ; Humans ; Meiosis/*physiology ; Nuclear Proteins ; Saccharomycetales/genetics/physiology ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Functional requirement for class I MHC in CNS development and plasticity (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-12-16
    Description: Class I major histocompatibility complex (class I MHC) molecules, known to be important for immune responses to antigen, are expressed also by neurons that undergo activity-dependent, long-term structural and synaptic modifications. Here, we show that in mice genetically deficient for cell surface class I MHC or for a class I MHC receptor component, CD3zeta, refinement of connections between retina and central targets during development is incomplete. In the hippocampus of adult mutants, N-methyl-D-aspartate receptor-dependent long-term potentiation (LTP) is enhanced, and long-term depression (LTD) is absent. Specific class I MHC messenger RNAs are expressed by distinct mosaics of neurons, reflecting a potential for diverse neuronal functions. These results demonstrate an important role for these molecules in the activity-dependent remodeling and plasticity of connections in the developing and mature mammalian central nervous system (CNS).〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2175035/" 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/PMC2175035/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huh, G S -- Boulanger, L M -- Du, H -- Riquelme, P A -- Brotz, T M -- Shatz, C J -- 1F32EY07016/EY/NEI NIH HHS/ -- EY06912/EY/NEI NIH HHS/ -- F32 EY007016/EY/NEI NIH HHS/ -- F32 EY007016-02/EY/NEI NIH HHS/ -- F32 EY007016-03/EY/NEI NIH HHS/ -- MH48108/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2000 Dec 15;290(5499):2155-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA. gshuh@alum.mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11118151" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD3/genetics/*physiology ; Brain/growth & development/*physiology ; Excitatory Postsynaptic Potentials ; Gene Expression Profiling ; Genes, MHC Class I ; Geniculate Bodies/physiology ; Hippocampus/growth & development/physiology ; Histocompatibility Antigens Class I/genetics/*physiology ; In Situ Hybridization ; Long-Term Potentiation ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Mutant Strains ; Neural Pathways ; *Neuronal Plasticity ; Neurons/*physiology ; Receptors, GABA-A/metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism ; Retina/growth & development/physiology ; Retinal Ganglion Cells/physiology ; Signal Transduction ; Synapses/*physiology ; Synaptic Transmission ; Visual Pathways
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 6
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    Reversal of antipsychotic-induced working memory deficits by short-term dopamine D1 receptor stimulation (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-03-17
    Description: Chronic blockade of dopamine D2 receptors, a common mechanism of action for antipsychotic drugs, down-regulates D1 receptors in the prefrontal cortex and, as shown here, produces severe impairments in working memory. These deficits were reversed in monkeys by short-term coadministration of a D1 agonist, ABT 431, and this improvement was sustained for more than a year after cessation of D1 treatment. These findings indicate that pharmacological modulation of the D1 signaling pathway can produce long-lasting changes in functional circuits underlying working memory. Resetting this pathway by brief exposure to the agonist may provide a valuable strategy for therapeutic intervention in schizophrenia and other dopamine dysfunctional states.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Castner, S A -- Williams, G V -- Goldman-Rakic, P S -- P01DA10160/DA/NIDA NIH HHS/ -- P50MH44866/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2000 Mar 17;287(5460):2020-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Neurobiology, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10720329" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antipsychotic Agents/*pharmacology ; Cyclic AMP/metabolism ; Dopamine/metabolism ; Dopamine Agonists/*pharmacology ; Dopamine Antagonists/pharmacology ; Down-Regulation ; Female ; Haloperidol/*pharmacology ; Haplorhini ; Memory/*drug effects ; Prefrontal Cortex/drug effects/metabolism ; Psychomotor Performance/drug effects ; Pyridines/*pharmacology ; Receptors, Dopamine D1/agonists/*metabolism ; Signal Transduction ; Tetrahydronaphthalenes/*pharmacology ; Time Factors
    Print ISSN: 0036-8075
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  • 7
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    Accommodating phylogenetic uncertainty in evolutionary studies (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-07-06
    Description: Many evolutionary studies use comparisons across species to detect evidence of natural selection and to examine the rate of character evolution. Statistical analyses in these studies are usually performed by means of a species phylogeny to accommodate the effects of shared evolutionary history. The phylogeny is usually treated as known without error; this assumption is problematic because inferred phylogenies are subject to both stochastic and systematic errors. We describe methods for accommodating phylogenetic uncertainty in evolutionary studies by means of Bayesian inference. The methods are computationally intensive but general enough to be applied in most comparative evolutionary studies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huelsenbeck, J P -- Rannala, B -- Masly, J P -- R01-HG01988/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2000 Jun 30;288(5475):2349-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of Rochester, Rochester, NY 14627, USA. johnh@brahms.biology.rochester.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10875916" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Aphids/genetics ; Base Sequence ; Bayes Theorem ; *Biological Evolution ; DNA, Mitochondrial/genetics ; *Evolution, Molecular ; Markov Chains ; Monte Carlo Method ; *Phylogeny ; Probability ; Stochastic Processes
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 8
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    Activation of the DNA replication checkpoint through RNA synthesis by primase (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-09-23
    Description: When DNA replication is inhibited during the synthesis (S) phase of the cell cycle, a signaling pathway (checkpoint) is activated that serves to prevent mitosis from initiating before completion of replication. This replication checkpoint acts by down-regulating the activity of the mitotic inducer cdc2-cyclin B. Here, we report the relation between chromatin structure and induction of the replication checkpoint. Chromatin was competent to initiate a checkpoint response only after the DNA was unwound and DNA polymerase alpha had been loaded. Checkpoint induction did not require new DNA synthesis on the unwound template strand but did require RNA primer synthesis by primase. These findings identify the RNA portion of the primer as an important component of the signal that activates the replication checkpoint.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Michael, W M -- Ott, R -- Fanning, E -- Newport, J -- 52948/PHS HHS/ -- R01GM33523-16/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2000 Sep 22;289(5487):2133-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of California, San Diego, La Jolla, CA 92093-0349, USA. matt@mcb.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11000117" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aphidicolin/pharmacology ; *CDC2-CDC28 Kinases ; Carrier Proteins/metabolism ; Chromatin/*metabolism ; Cyclin E/metabolism ; Cyclin-Dependent Kinase 2 ; Cyclin-Dependent Kinases/metabolism ; DNA Helicases/metabolism ; DNA Polymerase I/antagonists & inhibitors/metabolism ; DNA Primase/*metabolism ; *DNA Replication/drug effects ; DNA, Single-Stranded/metabolism ; DNA-Binding Proteins/metabolism ; Mitosis ; Nuclear Proteins/metabolism ; Phosphorylation ; Protein Kinases/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; RNA/*biosynthesis ; Recombinant Proteins/metabolism ; S Phase ; *Saccharomyces cerevisiae Proteins ; Signal Transduction ; Xenopus ; Xenopus Proteins
    Print ISSN: 0036-8075
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  • 9
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    Neurobiology. Receptors as kissing cousins (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-04-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Milligan, G -- New York, N.Y. -- Science. 2000 Apr 7;288(5463):65-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biochemistry and Molecular Biology, Institute of Biomedical and Life Sciences, University of Glasgow, Scotland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10766637" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclase Inhibitors ; Adenylyl Cyclases/metabolism ; Animals ; Cell Line ; Cerebral Cortex/metabolism ; Corpus Striatum/metabolism ; Dimerization ; Energy Transfer ; Fluorescence ; GTP-Binding Proteins/*metabolism ; Ligands ; Rats ; Receptor Cross-Talk ; Receptors, Dopamine D1/metabolism ; Receptors, Dopamine D2/agonists/*metabolism ; Receptors, Dopamine D5 ; Receptors, GABA-A/metabolism ; Receptors, Somatostatin/agonists/*metabolism ; Signal Transduction ; Somatostatin/metabolism
    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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    Two-amino acid molecular switch in an epithelial morphogen that regulates binding to two distinct receptors (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-10-20
    Description: Ectodysplasin, a member of the tumor necrosis factor family, is encoded by the anhidrotic ectodermal dysplasia (EDA) gene. Mutations in EDA give rise to a clinical syndrome characterized by loss of hair, sweat glands, and teeth. EDA-A1 and EDA-A2 are two isoforms of ectodysplasin that differ only by an insertion of two amino acids. This insertion functions to determine receptor binding specificity, such that EDA-A1 binds only the receptor EDAR, whereas EDA-A2 binds only the related, but distinct, X-linked ectodysplasin-A2 receptor (XEDAR). In situ binding and organ culture studies indicate that EDA-A1 and EDA-A2 are differentially expressed and play a role in epidermal morphogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yan, M -- Wang, L C -- Hymowitz, S G -- Schilbach, S -- Lee, J -- Goddard, A -- de Vos, A M -- Gao, W Q -- Dixit, V M -- New York, N.Y. -- Science. 2000 Oct 20;290(5491):523-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Oncology, Genentech, 1 DNA Way, South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11039935" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Binding Sites ; Cell Line ; DNA-Binding Proteins/metabolism ; Ectodermal Dysplasia/genetics ; Ectodysplasins ; Epidermis/embryology/*metabolism ; Humans ; *I-kappa B Proteins ; In Situ Hybridization ; Ligands ; Membrane Proteins/*chemistry/*metabolism ; Mice ; Models, Molecular ; Molecular Sequence Data ; Morphogenesis ; NF-kappa B/metabolism ; Phosphorylation ; Point Mutation ; Protein Conformation ; Proteins/metabolism ; Receptors, Cell Surface/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; TNF Receptor-Associated Factor 6 ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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