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  • Animals  (13)
  • Nucleic acid structure, RNA characterisation and manipulation, Computational Methods
  • Pathogens & Pathogenicity
  • Physics (General)
  • 2015-2019  (15)
  • 1995-1999  (8)
  • 1
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    Isolation and identification of nematode-antagonistic compounds from the fungus Aspergillus candidus (2016)
    Oxford University Press
    Details
    Publication Date: 2016-02-20
    Description: Culture medium from an isolate of the fungus Aspergillus candidus was extracted, fractionated and examined to discover compounds antagonistic to plant-parasitic nematodes that are important pathogens of agricultural crops. Column, thin layer and preparative chromatographies and spectral and elemental analyses, were used to isolate and identify two major constituents of an active fraction (Fraction F) obtained from the medium. Compound 1 was identified as 2-hydroxypropane-1, 2, 3-tricarboxylic acid (citric acid). Compound 2 was identified as 3-hydroxy-5-methoxy-3-(methoxycarbonyl)-5-oxopentanoic acid, an isomer of 1, 2-dimethyl citrate. Compound 1 and a citric acid standard, each tested at 50 mg mL –1 in water, decreased hatch from eggs of the plant-parasitic nematode Meloidogyne incognita by more than 94%, and completely immobilized second-stage juveniles after 4–6 days exposure. Fraction F and Compounds 1 and 2 decreased the mobility of adults of the plant-parasitic nematode Ditylenchus destructor in vitro . Fraction F (25 mg mL –1 ) inhibited mobility 〉99% at 72 hrs. Compounds 1 and 2 (50 mg mL –1 ) each inhibited mobility more than 25% at 24 hr and more than 50% at 72 hr. This is the first assignment of nematode-antagonistic properties to specifically identified A. candidus metabolites.
    Keywords: Pathogens & Pathogenicity
    Print ISSN: 0378-1097
    Electronic ISSN: 1574-6968
    Topics: Biology
    Published by Oxford University Press
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  • 2
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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
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Dynamic control of CaMKII translocation and localization in hippocampal neurons by NMDA receptor stimulation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-02
    Description: Calcium-calmodulin-dependent protein kinase II (CaMKII) is thought to increase synaptic strength by phosphorylating postsynaptic density (PSD) ion channels and signaling proteins. It is shown that N-methyl-D-aspartate (NMDA) receptor stimulation reversibly translocates green fluorescent protein-tagged CaMKII from an F-actin-bound to a PSD-bound state. The translocation time was controlled by the ratio of expressed beta-CaMKII to alpha-CaMKII isoforms. Although F-actin dissociation into the cytosol required autophosphorylation of or calcium-calmodulin binding to beta-CaMKII, PSD translocation required binding of calcium-calmodulin to either the alpha- or beta-CaMKII subunits. Autophosphorylation of CaMKII indirectly prolongs its PSD localization by increasing the calmodulin-binding affinity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shen, K -- Meyer, T -- GM-48113/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Apr 2;284(5411):162-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology and Department of Pharmacology and Cancer Biology, Box 3709, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10102820" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Animals ; Calcium/pharmacology ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Cells, Cultured ; Cytosol/metabolism ; Dendrites/*enzymology ; Electric Stimulation ; Glutamic Acid/pharmacology ; Green Fluorescent Proteins ; Hippocampus/cytology/*enzymology ; Isoenzymes/metabolism ; Luminescent Proteins ; Microscopy, Fluorescence ; Nerve Tissue Proteins/analysis ; Neurons/*enzymology ; Phosphorylation ; Rats ; Receptors, N-Methyl-D-Aspartate/*metabolism ; Synapses/*enzymology ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 4
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    Elementary calcium-release units induced by inositol trisphosphate (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-06-13
    Description: The extent to which inositol 1,4,5-trisphosphate (InsP3)-induced calcium signals are localized is a critical parameter for understanding the mechanism of effector activation. The spatial characteristics of InsP3-mediated calcium signals were determined by targeting a dextran-based calcium indicator to intracellular membranes through the in situ addition of a geranylgeranyl lipid group. Elementary calcium-release events observed with this indicator typically lasted less than 33 milliseconds, had diameters less than 2 micrometers, and were uncoupled from each other by the calcium buffer EGTA. Cellwide calcium transients are likely to result from synchronized triggering of such local release events, suggesting that calcium-dependent effector proteins could be selectively activated by localization near sites of local calcium release.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Horne, J H -- Meyer, T -- GM-51457/GM/NIGMS NIH HHS/ -- P01-HL-47053/HL/NHLBI NIH HHS/ -- R01-GM-48113/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Jun 13;276(5319):1690-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9180077" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Calcium Channels/metabolism ; Cytosol/metabolism ; Egtazic Acid/pharmacology ; Electroporation ; Fluorescent Dyes ; Inositol 1,4,5-Trisphosphate/*pharmacology ; Intracellular Membranes/*metabolism ; Kinetics ; Microscopy, Confocal ; Microscopy, Fluorescence ; Organic Chemicals ; Peptides/metabolism ; Rats ; Signal Transduction ; Tumor Cells, Cultured
    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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    A comprehensive comparison of general RNA-RNA interaction prediction methods (2016)
    Oxford University Press
    Details
    Publication Date: 2016-04-21
    Description: RNA–RNA interactions are fast emerging as a major functional component in many newly discovered non-coding RNAs. Basepairing is believed to be a major contributor to the stability of these intermolecular interactions, much like intramolecular basepairs formed in RNA secondary structure. As such, using algorithms similar to those for predicting RNA secondary structure, computational methods have been recently developed for the prediction of RNA–RNA interactions. We provide the first comprehensive comparison comprising 14 methods that predict general intermolecular basepairs. To evaluate these, we compile an extensive data set of 54 experimentally confirmed fungal snoRNA–rRNA interactions and 102 bacterial sRNA–mRNA interactions. We test the performance accuracy of all methods, evaluating the effects of tool settings, sequence length, and multiple sequence alignment usage and quality. Our results show that—unlike for RNA secondary structure prediction—the overall best performing tools are non-comparative energy-based tools utilizing accessibility information that predict short interactions on this data set. Furthermore, we find that maintaining high accuracy across biologically different data sets and increasing input lengths remains a huge challenge, causing implications for de novo transcriptome-wide searches. Finally, we make our interaction data set publicly available for future development and benchmarking efforts.
    Keywords: Nucleic acid structure, RNA characterisation and manipulation, Computational Methods
    Print ISSN: 0305-1048
    Electronic ISSN: 1362-4962
    Topics: Biology
    Published by Oxford University Press
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  • 6
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    A p16INK4a-insensitive CDK4 mutant targeted by cytolytic T lymphocytes in a human melanoma (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-09-01
    Description: A mutated cyclin-dependent kinase 4 (CDK4) was identified as a tumor-specific antigen recognized by HLA-A2. 1-restricted autologous cytolytic T lymphocytes (CTLs) in a human melanoma. The mutated CDK4 allele was present in autologous cultured melanoma cells and metastasis tissue, but not in the patient's lymphocytes. The mutation, an arginine-to-cysteine exchange at residue 24, was part of the CDK4 peptide recognized by CTLs and prevented binding of the CDK4 inhibitor p16INK4a, but not of p21 or of p27KIP1. The same mutation was found in one additional melanoma among 28 melanomas analyzed. These results suggest that mutation of CDK4 can create a tumor-specific antigen and can disrupt the cell-cycle regulation exerted by the tumor suppressor p16INK4a.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wolfel, T -- Hauer, M -- Schneider, J -- Serrano, M -- Wolfel, C -- Klehmann-Hieb, E -- De Plaen, E -- Hankeln, T -- Meyer zum Buschenfelde, K H -- Beach, D -- New York, N.Y. -- Science. 1995 Sep 1;269(5228):1281-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medizinische Klinik und Poliklinik, Johannes Gutenberg-Universitat, Mainz, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7652577" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Carrier Proteins/metabolism/*pharmacology ; *Cell Cycle Proteins ; Cell Line ; Cloning, Molecular ; Cyclin-Dependent Kinase 4 ; Cyclin-Dependent Kinase Inhibitor p15 ; Cyclin-Dependent Kinase Inhibitor p16 ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclin-Dependent Kinase Inhibitor p27 ; *Cyclin-Dependent Kinases ; Cyclins/metabolism/pharmacology ; HLA-A2 Antigen/immunology ; Humans ; Melanoma/enzymology/*immunology ; Microtubule-Associated Proteins/metabolism/pharmacology ; Molecular Sequence Data ; Point Mutation ; Polymerase Chain Reaction ; Protein-Serine-Threonine Kinases/antagonists & ; inhibitors/genetics/*immunology/metabolism ; *Proto-Oncogene Proteins ; T-Lymphocytes, Cytotoxic/*immunology ; Transfection ; Tumor Cells, Cultured ; *Tumor Suppressor Proteins
    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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  • 7
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    Enhanced DNA-binding activity of a Stat3-related protein in cells transformed by the Src oncoprotein (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-07-07
    Description: Cytokines and growth factors induce tyrosine phosphorylation of signal transducers and activators of transcription (STATs) that directly activate gene expression. Cells stably transformed by the Src oncogene tyrosine kinase were examined for STAT protein activation. Assays of electrophoretic mobility, DNA-binding specificity, and antigenicity indicated that Stat3 or a closely related STAT family member was constitutively activated by the Src oncoprotein. Induction of this DNA-binding activity was accompanied by tyrosine phosphorylation of Stat3 and correlated with Src transformation. These findings demonstrate that Src can activate STAT signaling pathways and raise the possibility that Stat3 contributes to oncogenesis by Src.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, C L -- Meyer, D J -- Campbell, G S -- Larner, A C -- Carter-Su, C -- Schwartz, J -- Jove, R -- CA55652/CA/NCI NIH HHS/ -- DK34171/DK/NIDDK NIH HHS/ -- R01 DK034171/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1995 Jul 7;269(5220):81-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor 48109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7541555" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Line, Transformed ; *Cell Transformation, Neoplastic ; DNA/*metabolism ; DNA-Binding Proteins/*metabolism ; Growth Inhibitors/pharmacology ; Interferon-gamma/pharmacology ; *Interleukin-6 ; Leukemia Inhibitory Factor ; Lymphokines/pharmacology ; Mice ; Molecular Sequence Data ; Oncogene Protein pp60(v-src)/*physiology ; Phosphorylation ; Phosphotyrosine ; STAT3 Transcription Factor ; *Signal Transduction ; Trans-Activators/*metabolism ; Tyrosine/analogs & derivatives/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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  • 8
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    Sex-specific assembly of a dosage compensation complex on the nematode X chromosome (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-06
    Description: In nematodes, flies, and mammals, dosage compensation equalizes X-chromosome gene expression between the sexes through chromosome-wide regulatory mechanisms that function in one sex to adjust the levels of X-linked transcripts. Here, a dosage compensation complex was identified in the nematode Caenorhabditis elegans that reduces transcript levels from the two X chromosomes in hermaphrodites. This complex contains at least four proteins, including products of the dosage compensation genes dpy-26 and dpy-27. Specific localization of the complex to the hermaphrodite X chromosomes is conferred by XX-specific regulatory genes that coordinately control both sex determination and dosage compensation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chuang, P T -- Lieb, J D -- Meyer, B J -- GM30702/GM/NIGMS NIH HHS/ -- T32 GM07127/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1996 Dec 6;274(5293):1736-9.〈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/8939870" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/*genetics/metabolism ; *Caenorhabditis elegans Proteins ; Carrier Proteins/analysis/chemistry/*metabolism ; Disorders of Sex Development ; *Dosage Compensation, Genetic ; Electrophoresis, Polyacrylamide Gel ; Female ; Genes, Helminth ; Genes, Regulator ; Helminth Proteins/analysis/chemistry/*metabolism ; Male ; Nuclear Proteins/analysis/chemistry/*metabolism ; Precipitin Tests ; RNA, Helminth/metabolism ; RNA, Messenger/metabolism ; Sex Determination Analysis ; X Chromosome/chemistry/*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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  • 9
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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
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    CORAL REEFS. Genomic determinants of coral heat tolerance across latitudes (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-06-27
    Description: As global warming continues, reef-building corals could avoid local population declines through "genetic rescue" involving exchange of heat-tolerant genotypes across latitudes, but only if latitudinal variation in thermal tolerance is heritable. Here, we show an up-to-10-fold increase in odds of survival of coral larvae under heat stress when their parents come from a warmer lower-latitude location. Elevated thermal tolerance was associated with heritable differences in expression of oxidative, extracellular, transport, and mitochondrial functions that indicated a lack of prior stress. Moreover, two genomic regions strongly responded to selection for thermal tolerance in interlatitudinal crosses. These results demonstrate that variation in coral thermal tolerance across latitudes has a strong genetic basis and could serve as raw material for natural selection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dixon, Groves B -- Davies, Sarah W -- Aglyamova, Galina A -- Meyer, Eli -- Bay, Line K -- Matz, Mikhail V -- New York, N.Y. -- Science. 2015 Jun 26;348(6242):1460-2. doi: 10.1126/science.1261224.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Integrative Biology, University of Texas at Austin, 205 W. 24th Street C0990, Austin, TX 78712, USA. ; Department of Integrative Biology, Oregon State University, 3106 Cordley Hall, Corvallis, OR 97331, USA. ; Australian Institute of Marine Science, PMB 3, Townsville MC, Queensland 4810, Australia. l.bay@aims.gov.au matz@utexas.edu. ; Department of Integrative Biology, University of Texas at Austin, 205 W. 24th Street C0990, Austin, TX 78712, USA. l.bay@aims.gov.au matz@utexas.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26113720" target="_blank"〉PubMed〈/a〉
    Keywords: Acclimatization/*genetics ; Animals ; Anthozoa/*genetics/*physiology ; *Coral Reefs ; Extinction, Biological ; Gene Expression ; Gene Frequency ; Genetic Markers ; *Global Warming ; *Hot Temperature ; Larva/genetics/physiology ; Selection, Genetic ; Stress, Physiological/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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