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  • Mutation  (9)
  • American Association for the Advancement of Science (AAAS)  (9)
  • American Physical Society
  • Oxford University Press
  • Springer Nature
  • Wiley
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Keywords
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  • American Association for the Advancement of Science (AAAS)  (9)
  • American Physical Society
  • Oxford University Press
  • Springer Nature
  • Wiley
Years
  • 1
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    Dosage compensation proteins targeted to X chromosomes by a determinant of hermaphrodite fate (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-12
    Description: In many organisms, master control genes coordinately regulate sex-specific aspects of development. SDC-2 was shown to induce hermaphrodite sexual differentiation and activate X chromosome dosage compensation in Caenorhabditis elegans. To control these distinct processes, SDC-2 acts as a strong gene-specific repressor and a weaker chromosome-wide repressor. To initiate hermaphrodite development, SDC-2 associates with the promoter of the male sex-determining gene her-1 to repress its transcription. To activate dosage compensation, SDC-2 triggers assembly of a specialized protein complex exclusively on hermaphrodite X chromosomes to reduce gene expression by half. SDC-2 can localize to X chromosomes without other components of the dosage compensation complex, suggesting that SDC-2 targets dosage compensation machinery to X chromosomes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dawes, H E -- Berlin, D S -- Lapidus, D M -- Nusbaum, C -- Davis, T L -- Meyer, B J -- GM30702/GM/NIGMS NIH HHS/ -- T32 GM07127/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Jun 11;284(5421):1800-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720-3204, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10364546" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/embryology/*genetics/physiology ; *Caenorhabditis elegans Proteins ; *DNA-Binding Proteins ; Disorders of Sex Development ; *Dosage Compensation, Genetic ; Female ; Gene Expression Regulation, Developmental ; Genes, Helminth ; Helminth Proteins/genetics/*physiology ; Male ; Molecular Sequence Data ; Mutation ; Promoter Regions, Genetic ; Repressor Proteins/genetics/*physiology ; *Sex Determination Processes ; Transgenes ; X Chromosome/genetics/*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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  • 2
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    Rapid progression to AIDS in HIV+ individuals with a structural variant of the chemokine receptor CX3CR1 (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-03-24
    Description: Human immunodeficiency virus (HIV) enters cells in vitro via CD4 and a coreceptor. Which of 15 known coreceptors are important in vivo is poorly defined but may be inferred from disease-modifying mutations, as for CCR5. Here two single nucleotide polymorphisms are described in Caucasians in CX3CR1, an HIV coreceptor and leukocyte chemotactic/adhesion receptor for the chemokine fractalkine. HIV-infected patients homozygous for CX3CR1-I249 M280, a variant haplotype affecting two amino acids (isoleucine-249 and methionine-280), progressed to AIDS more rapidly than those with other haplotypes. Functional CX3CR1 analysis showed that fractalkine binding is reduced among patients homozygous for this particular haplotype. Thus, CX3CR1-I249 M280 is a recessive genetic risk factor in HIV/AIDS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Faure, S -- Meyer, L -- Costagliola, D -- Vaneensberghe, C -- Genin, E -- Autran, B -- Delfraissy, J F -- McDermott, D H -- Murphy, P M -- Debre, P -- Theodorou, I -- Combadiere, C -- New York, N.Y. -- Science. 2000 Mar 24;287(5461):2274-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire d'Immunologie Cellulaire et Tissulaire, Centre National de la Recherche Scientifique UMR 7627, Hopital Pitie-Salpetriere, Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10731151" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/genetics/*physiopathology/virology ; Case-Control Studies ; Chemokine CX3CL1 ; *Chemokines, CX3C ; Chemokines, CXC/metabolism ; Chromosomes, Human, Pair 3 ; Cohort Studies ; Disease Progression ; European Continental Ancestry Group/genetics ; Genetic Variation ; Genotype ; HIV/physiology ; HIV Infections/genetics/*physiopathology/virology ; Haplotypes ; Homozygote ; Humans ; Leukocytes, Mononuclear/metabolism ; Linkage Disequilibrium ; Membrane Proteins/metabolism ; Mutation ; Polymorphism, Restriction Fragment Length ; *Polymorphism, Single Nucleotide ; Polymorphism, Single-Stranded Conformational ; Receptors, Cytokine/*genetics/*physiology ; Receptors, HIV/*genetics/*physiology ; Survival Analysis
    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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    RTEL-1 enforces meiotic crossover interference and homeostasis (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-03-06
    Description: Meiotic crossovers (COs) are tightly regulated to ensure that COs on the same chromosome are distributed far apart (crossover interference, COI) and that at least one CO is formed per homolog pair (CO homeostasis). CO formation is controlled in part during meiotic double-strand break (DSB) creation in Caenorhabditis elegans, but a second level of control must also exist because meiotic DSBs outnumber COs. We show that the antirecombinase RTEL-1 is required to prevent excess meiotic COs, probably by promoting meiotic synthesis-dependent strand annealing. Two distinct classes of meiotic COs are increased in rtel-1 mutants, and COI and homeostasis are compromised. We propose that RTEL-1 implements the second level of CO control by promoting noncrossovers.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4770885/" 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/PMC4770885/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Youds, Jillian L -- Mets, David G -- McIlwraith, Michael J -- Martin, Julie S -- Ward, Jordan D -- ONeil, Nigel J -- Rose, Ann M -- West, Stephen C -- Meyer, Barbara J -- Boulton, Simon J -- Canadian Institutes of Health Research/Canada -- Cancer Research UK/United Kingdom -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Mar 5;327(5970):1254-8. doi: 10.1126/science.1183112.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉DNA Damage Response Laboratory, London Research Institute, Cancer Research UK, Clare Hall, South Mimms, EN6 3LD, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20203049" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/*genetics/physiology ; Caenorhabditis elegans Proteins/genetics/*metabolism ; Chromatids/genetics ; Chromosomal Proteins, Non-Histone/genetics/metabolism ; *Crossing Over, Genetic ; DNA Breaks, Double-Stranded ; DNA Helicases/genetics/*metabolism ; DNA Repair ; DNA, Helminth/genetics/metabolism ; Homeostasis ; *Meiosis ; Mutation ; Polymorphism, Single Nucleotide ; X Chromosome/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    DPY-26, a link between dosage compensation and meiotic chromosome segregation in the nematode (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-06
    Description: The DPY-26 protein is required in the nematode Caenorhabditis elegans for X-chromosome dosage compensation as well as for proper meiotic chromosome segregation. DPY-26 was shown to mediate both processes through its association with chromosomes. In somatic cells, DPY-26 associates specifically with hermaphrodite X chromosomes to reduce their transcript levels. In germ cells, DPY-26 associates with all meiotic chromosomes to mediate its role in chromosome segregation. The X-specific localization of DPY-26 requires two dosage compensation proteins (DPY-27 and DPY-30) and two proteins that coordinately control both sex determination and dosage compensation (SDC-2 and SDC-3).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lieb, J D -- Capowski, E E -- Meneely, P -- Meyer, B J -- GM30702/GM/NIGMS NIH HHS/ -- HD24324/HD/NICHD NIH HHS/ -- T32 GM07127/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1996 Dec 6;274(5293):1732-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8939869" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/embryology/genetics/*physiology ; *Caenorhabditis elegans Proteins ; Carrier Proteins/physiology ; Cell Nucleus/chemistry ; Chromosomes/*physiology ; Disorders of Sex Development ; *Dosage Compensation, Genetic ; Embryonic Development ; Female ; Gene Expression ; Genes, Helminth ; Germ Cells/physiology ; Helminth Proteins/analysis/genetics/*physiology ; Male ; *Meiosis ; Molecular Sequence Data ; Mutation ; Nuclear Proteins/physiology ; X Chromosome/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 5
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    Activation of Gal4p by galactose-dependent interaction of galactokinase and Gal80p (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-06-14
    Description: Yeast galactokinase (Gal1p) is an enzyme and a regulator of transcription. In addition to phosphorylating galactose, Gal1p activates Gal4p, the activator of GAL genes, but the mechanism of this regulation has been unclear. Here, biochemical and genetic evidence is presented to show that Gal1p activates Gal4p by direct interaction with the Gal4p inhibitor Gal80p. Interaction requires galactose, adenosine triphosphate, and the regulatory function of Gal1p. These data indicate that Gal1p-Gal80p complex formation results in the inactivation of Gal80p, thereby transmitting the galactose signal to Gal4p.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zenke, F T -- Engles, R -- Vollenbroich, V -- Meyer, J -- Hollenberg, C P -- Breunig, K D -- New York, N.Y. -- Science. 1996 Jun 14;272(5268):1662-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut fur Mikrobiologie, Heinrich-Heine-Universitat Dusseldorf, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8658143" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Coenzymes/metabolism ; DNA-Binding Proteins ; Fungal Proteins/*metabolism ; Galactokinase/genetics/*metabolism ; Galactose/*metabolism ; Kluyveromyces/genetics/metabolism ; Molecular Sequence Data ; Mutation ; Repressor Proteins/*metabolism ; Saccharomyces cerevisiae/genetics/*metabolism ; *Saccharomyces cerevisiae Proteins ; Signal Transduction ; Transcription Factors/*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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  • 6
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    A protein phosphatase 2C involved in ABA signal transduction in Arabidopsis thaliana (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-03
    Description: The plant hormone abscisic acid (ABA) mediates various responses such as stomatal closure, the maintenance of seed dormancy, and the inhibition of plant growth. All three responses are affected in the ABA-insensitive mutant abi1 of Arabidopsis thaliana, suggesting that an early step in the signaling of ABA is controlled by the ABI1 locus. The ABI1 gene was cloned by chromosome walking, and a missense mutation was identified in the structural gene of the abi1 mutant. The ABI1 gene encodes a protein with high similarity to protein serine or threonine phosphatases of type 2C with the novel feature of a putative Ca2+ binding site. Thus, the control of the phosphorylation state of cell signaling components by the ABI1 product could mediate pleiotropic hormone responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meyer, K -- Leube, M P -- Grill, E -- New York, N.Y. -- Science. 1994 Jun 3;264(5164):1452-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Plant Sciences, Swiss Federal Institute of Technology, Zurich.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8197457" target="_blank"〉PubMed〈/a〉
    Keywords: Abscisic Acid/*pharmacology ; Amino Acid Sequence ; Arabidopsis/enzymology/genetics/*metabolism ; *Arabidopsis Proteins ; Binding Sites ; Calcium/metabolism ; Chromosome Walking ; Cloning, Molecular ; Genes, Plant ; Genetic Markers ; Molecular Sequence Data ; Mutation ; Phosphoprotein Phosphatases/chemistry/genetics/*metabolism ; Plants, Genetically Modified ; *Signal Transduction
    Print ISSN: 0036-8075
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  • 7
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    Conformational switch of syntaxin-1 controls synaptic vesicle fusion (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-08-16
    Description: During synaptic vesicle fusion, the soluble N-ethylmaleimide-sensitive factor-attachment protein receptor (SNARE) protein syntaxin-1 exhibits two conformations that both bind to Munc18-1: a "closed" conformation outside the SNARE complex and an "open" conformation in the SNARE complex. Although SNARE complexes containing open syntaxin-1 and Munc18-1 are essential for exocytosis, the function of closed syntaxin-1 is unknown. We generated knockin/knockout mice that expressed only open syntaxin-1B. Syntaxin-1B(Open) mice were viable but succumbed to generalized seizures at 2 to 3 months of age. Binding of Munc18-1 to syntaxin-1 was impaired in syntaxin-1B(Open) synapses, and the size of the readily releasable vesicle pool was decreased; however, the rate of synaptic vesicle fusion was dramatically enhanced. Thus, the closed conformation of syntaxin-1 gates the initiation of the synaptic vesicle fusion reaction, which is then mediated by SNARE-complex/Munc18-1 assemblies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3235364/" 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/PMC3235364/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gerber, Stefan H -- Rah, Jong-Cheol -- Min, Sang-Won -- Liu, Xinran -- de Wit, Heidi -- Dulubova, Irina -- Meyer, Alexander C -- Rizo, Josep -- Arancillo, Marife -- Hammer, Robert E -- Verhage, Matthijs -- Rosenmund, Christian -- Sudhof, Thomas C -- NS051262/NS/NINDS NIH HHS/ -- NS37200/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Sep 12;321(5895):1507-10. doi: 10.1126/science.1163174. Epub 2008 Aug 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, University of Texas Southwestern Medical Center, Dallas, TX 75390-9111, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18703708" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Epilepsy/etiology ; Excitatory Postsynaptic Potentials ; Membrane Fusion ; Mice ; Mice, Knockout ; Munc18 Proteins/metabolism ; Mutation ; Protein Conformation ; Protein Structure, Tertiary ; SNARE Proteins/metabolism ; Sucrose/metabolism ; Synapses/physiology ; Synaptic Vesicles/*physiology/ultrastructure ; Syntaxin 1/*chemistry/genetics/*metabolism
    Print ISSN: 0036-8075
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  • 8
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    Mps1 and Ipl1/Aurora B act sequentially to correctly orient chromosomes on the meiotic spindle of budding yeast (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-02-02
    Description: The conserved kinases Mps1 and Ipl1/Aurora B are critical for enabling chromosomes to attach to microtubules so that partner chromosomes will be segregated correctly from each other, but the precise roles of these kinases have been unclear. We imaged live yeast cells to elucidate the stages of chromosome-microtubule interactions and their regulation by Ipl1 and Mps1 through meiosis I. Ipl1 was found to release kinetochore-microtubule (kMT) associations after meiotic entry, liberating chromosomes to begin homologous pairing. Surprisingly, most chromosome pairs began their spindle interactions with incorrect kMT attachments. Ipl1 released these improper connections, whereas Mps1 triggered the formation of new force-generating microtubule attachments. This microtubule release and reattachment cycle could prevent catastrophic chromosome segregation errors in meiosis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3604795/" 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/PMC3604795/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meyer, Regis E -- Kim, Seoyoung -- Obeso, David -- Straight, Paul D -- Winey, Mark -- Dawson, Dean S -- GM-07135/GM/NIGMS NIH HHS/ -- GM087377/GM/NIGMS NIH HHS/ -- R01 GM051312/GM/NIGMS NIH HHS/ -- R01 GM087377/GM/NIGMS NIH HHS/ -- T32 GM007135/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2013 Mar 1;339(6123):1071-4. doi: 10.1126/science.1232518. Epub 2013 Jan 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Cycle and Cancer Biology, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23371552" target="_blank"〉PubMed〈/a〉
    Keywords: Aurora Kinases ; Chromosome Segregation/genetics/*physiology ; Chromosomes, Fungal/*genetics ; Intracellular Signaling Peptides and Proteins/genetics/*physiology ; Kinetochores/enzymology ; Meiosis/genetics/*physiology ; Microtubules/enzymology ; Mutation ; Protein-Serine-Threonine Kinases/genetics/*physiology ; Saccharomyces cerevisiae/enzymology/genetics/*physiology ; Saccharomyces cerevisiae Proteins/genetics/*physiology
    Print ISSN: 0036-8075
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  • 9
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    An ancient defense system eliminates unfit cells from developing tissues during cell competition (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-12-06
    Description: Developing tissues that contain mutant or compromised cells present risks to animal health. Accordingly, the appearance of a population of suboptimal cells in a tissue elicits cellular interactions that prevent their contribution to the adult. Here we report that this quality control process, cell competition, uses specific components of the evolutionarily ancient and conserved innate immune system to eliminate Drosophila cells perceived as unfit. We find that Toll-related receptors (TRRs) and the cytokine Spatzle (Spz) lead to NFkappaB-dependent apoptosis. Diverse "loser" cells require different TRRs and NFkappaB factors and activate distinct pro-death genes, implying that the particular response is stipulated by the competitive context. Our findings demonstrate a functional repurposing of components of TRRs and NFkappaB signaling modules in the surveillance of cell fitness during development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meyer, S N -- Amoyel, M -- Bergantinos, C -- de la Cova, C -- Schertel, C -- Basler, K -- Johnston, L A -- P40OD018537/OD/NIH HHS/ -- R01 GM078464/GM/NIGMS NIH HHS/ -- R01-GM084947/GM/NIGMS NIH HHS/ -- R21 HD067918/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2014 Dec 5;346(6214):1258236. doi: 10.1126/science.1258236.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular Life Sciences, University of Zurich, Zurich, Switzerland. ; Department of Genetics and Development, Columbia University, New York, NY 10032, USA. ; Institute of Molecular Life Sciences, University of Zurich, Zurich, Switzerland. konrad.basler@imls.uzh.ch lj180@columbia.edu. ; Department of Genetics and Development, Columbia University, New York, NY 10032, USA. konrad.basler@imls.uzh.ch lj180@columbia.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25477468" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis/genetics/*immunology ; Cell Communication/*immunology ; Drosophila Proteins/genetics/metabolism ; Drosophila melanogaster/cytology/genetics/growth & development ; Immunity, Innate/genetics/*immunology ; Mutation ; NF-kappa B/genetics/*metabolism ; Neuropeptides/genetics ; Toll-Like Receptors/genetics/*metabolism ; Transcription Factors/metabolism ; Transcription, Genetic
    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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