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  • Articles  (53)
  • Phenotype  (53)
  • 2000-2004  (53)
  • 2003  (53)
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  • 1
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2003-09-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gurian-Sherman, Doug -- New York, N.Y. -- Science. 2003 Sep 26;301(5641):1845; author reply 1845.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14512604" target="_blank"〉PubMed〈/a〉
    Keywords: Crops, Agricultural/*genetics/standards ; Genetic Engineering ; Government Regulation ; Phenotype ; *Plants, Genetically Modified ; Risk Assessment ; United States ; *United States Department of Agriculture ; *United States Environmental Protection Agency
    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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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2003-12-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, Kathryn -- New York, N.Y. -- Science. 2003 Nov 28;302(5650):1499.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14645825" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; *Biological Evolution ; Desert Climate ; Ecosystem ; Environment ; Genes, Plant ; Helianthus/*genetics/growth & development/physiology ; History, 20th Century ; History, 21st Century ; *Hybridization, Genetic ; Mutation ; Phenotype ; Sodium Chloride/pharmacology ; United States
    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
    Publication Date: 2003-05-06
    Description: Degenerative disorders of motor neurons include a range of progressive fatal diseases such as amyotrophic lateral sclerosis (ALS), spinal-bulbar muscular atrophy (SBMA), and spinal muscular atrophy (SMA). Although the causative genetic alterations are known for some cases, the molecular basis of many SMA and SBMA-like syndromes and most ALS cases is unknown. Here we show that missense point mutations in the cytoplasmic dynein heavy chain result in progressive motor neuron degeneration in heterozygous mice, and in homozygotes this is accompanied by the formation of Lewy-like inclusion bodies, thus resembling key features of human pathology. These mutations exclusively perturb neuron-specific functions of dynein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hafezparast, Majid -- Klocke, Rainer -- Ruhrberg, Christiana -- Marquardt, Andreas -- Ahmad-Annuar, Azlina -- Bowen, Samantha -- Lalli, Giovanna -- Witherden, Abi S -- Hummerich, Holger -- Nicholson, Sharon -- Morgan, P Jeffrey -- Oozageer, Ravi -- Priestley, John V -- Averill, Sharon -- King, Von R -- Ball, Simon -- Peters, Jo -- Toda, Takashi -- Yamamoto, Ayumu -- Hiraoka, Yasushi -- Augustin, Martin -- Korthaus, Dirk -- Wattler, Sigrid -- Wabnitz, Philipp -- Dickneite, Carmen -- Lampel, Stefan -- Boehme, Florian -- Peraus, Gisela -- Popp, Andreas -- Rudelius, Martina -- Schlegel, Juergen -- Fuchs, Helmut -- Hrabe de Angelis, Martin -- Schiavo, Giampietro -- Shima, David T -- Russ, Andreas P -- Stumm, Gabriele -- Martin, Joanne E -- Fisher, Elizabeth M C -- New York, N.Y. -- Science. 2003 May 2;300(5620):808-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurodegenerative Disease, Institute of Neurology, National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12730604" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anterior Horn Cells/pathology ; Apoptosis ; *Axonal Transport ; Cell Differentiation ; Cell Movement ; Central Nervous System/embryology ; Chromosome Mapping ; Dimerization ; Dyneins/chemistry/*genetics/*physiology ; Female ; Ganglia, Spinal/pathology ; Golgi Apparatus/metabolism/ultrastructure ; Heterozygote ; Homozygote ; Lewy Bodies/pathology ; Male ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Motor Neuron Disease/*genetics/pathology/physiopathology ; Motor Neurons/*physiology/ultrastructure ; Mutation ; Mutation, Missense ; *Nerve Degeneration ; Peptide Fragments/metabolism ; Phenotype ; Point Mutation ; Spinal Nerves/growth & development ; Tetanus Toxin/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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  • 4
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2003-02-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bray, Dennis -- New York, N.Y. -- Science. 2003 Feb 21;299(5610):1189-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Zoology, University of Cambridge, Cambridge CB2 3EJ, UK. d.bray@zoo.cam.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12595679" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Substitution ; Animals ; Antibody Diversity ; Escherichia coli Proteins/chemistry/genetics/metabolism ; Evolution, Molecular ; Genetic Variation ; Genomics ; Histones/chemistry/genetics/metabolism ; Humans ; Methylation ; Phenotype ; Potassium Channels/chemistry/genetics/metabolism ; Protein Conformation ; Protein Isoforms/chemistry/metabolism ; Protein Processing, Post-Translational ; Proteins/*chemistry/genetics/*metabolism ; Proteomics ; RNA Splicing ; Receptors, Cell Surface/chemistry/genetics/metabolism ; Selection, Genetic ; Troponin T/chemistry/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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  • 5
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2003-12-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Elena, Santiago F -- Sanjuan, Rafael -- New York, N.Y. -- Science. 2003 Dec 19;302(5653):2074-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Instituto de Biologia Molecular y Celular de Plantas, Consejo Superior de Investigaciones Cientificas-UPV, 46022 Valencia, Spain. sfelena@ibmcp.upv.es〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14684807" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptation, Physiological ; Animals ; *Biological Evolution ; Chlamydomonas/physiology ; Darkness ; *Ecosystem ; Environment ; *Genetic Variation ; Genotype ; Light ; Mutation ; Phenotype ; Pseudomonas fluorescens/genetics/*physiology ; RNA Viruses/physiology ; Selection, 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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  • 6
    Publication Date: 2003-08-16
    Description: Plants attacked by pathogens rapidly deposit callose, a beta-1,3-glucan, at wound sites. Traditionally, this deposition is thought to reinforce the cell wall and is regarded as a defense response. Surprisingly, here we found that powdery mildew resistant 4 (pmr4), a mutant lacking pathogen-induced callose, became resistant to pathogens, rather than more susceptible. This resistance was due to mutation of a callose synthase, resulting in a loss of the induced callose response. Double-mutant analysis indicated that blocking the salicylic acid (SA) defense signaling pathway was sufficient to restore susceptibility to pmr4 mutants. Thus, callose or callose synthase negatively regulates the SA pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nishimura, Marc T -- Stein, Monica -- Hou, Bi-Huei -- Vogel, John P -- Edwards, Herb -- Somerville, Shauna C -- New York, N.Y. -- Science. 2003 Aug 15;301(5635):969-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Plant Biology, Carnegie Institution, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12920300" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Arabidopsis/cytology/genetics/*metabolism/*microbiology ; Ascomycota/*physiology ; Cell Death ; Gene Expression Profiling ; Gene Expression Regulation, Plant ; Genes, Plant ; Glucans/metabolism ; Glucosyltransferases/*genetics/metabolism ; *Membrane Proteins ; Mutation ; Oligonucleotide Array Sequence Analysis ; Phenotype ; *Plant Diseases ; Plant Leaves/metabolism ; Salicylic Acid/*metabolism ; *Schizosaccharomyces pombe Proteins ; 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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  • 7
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2003-10-04
    Description: The success of the green revolution largely resulted from the creation of dwarf cultivars of wheat and rice, which had much higher yields than conventional crops. Characterization of these dwarf cultivars showed that the mutant genes were involved in either the synthesis or signaling of gibberellin, a plant growth hormone. In his Perspective, Salamini highlights new work (Multani et al.) that identifies the cause of dwarfism in agronomically important varieties of maize and sorghum. In these cases, dwarfism is caused by defective transport of another growth hormone called auxin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Salamini, Francesco -- New York, N.Y. -- Science. 2003 Oct 3;302(5642):71-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute of Breeding Research, 50829 Koln, Germany. salamini@mpiz-koeln.mpg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14526071" target="_blank"〉PubMed〈/a〉
    Keywords: Agriculture ; Arabidopsis/genetics/growth & development/metabolism ; Arabidopsis Proteins/genetics/metabolism ; Biological Transport ; Breeding ; *Genes, Plant ; Genetic Engineering ; Genome, Plant ; Indoleacetic Acids/*metabolism ; Light ; Mutation ; P-Glycoproteins/genetics/metabolism ; Phenotype ; Plant Proteins/genetics/metabolism ; Poaceae/genetics/growth & development/*metabolism ; Quantitative Trait Loci ; Zea mays/genetics/growth & development/*metabolism
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 2003-10-25
    Description: Many vertebrate organs adopt asymmetric positions with respect to the midline, but little is known about the cellular changes and tissue movements that occur downstream of left-right gene expression to produce this asymmetry. Here, we provide evidence that the looping of the zebrafish gut results from the asymmetric migration of the neighboring lateral plate mesoderm (LPM). Mutations that disrupt the epithelial structure of the LPM perturb this asymmetric migration and inhibit gut looping. Asymmetric LPM migration still occurs when the endoderm is ablated from the gut-looping region, suggesting that the LPM can autonomously provide a motive force for gut displacement. Finally, reducing left-sided Nodal activity randomizes the pattern of LPM migration and gut looping. These results reveal a cellular framework for the regulation of organ laterality by asymmetrically expressed genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Horne-Badovinac, Sally -- Rebagliati, Michael -- Stainier, Didier Y R -- New York, N.Y. -- Science. 2003 Oct 24;302(5645):662-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, Programs in Developmental Biology, Genetics, and Human Genetics, University of California, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14576439" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Body Patterning ; Cell Movement ; Cues ; Endoderm/physiology ; *Gene Expression Regulation, Developmental ; Guanylate Kinase ; Homeodomain Proteins/genetics/physiology ; Intestines/*embryology ; Isoenzymes ; Mesoderm/cytology/physiology ; Morphogenesis ; Mutation ; *Nuclear Proteins ; Nucleoside-Phosphate Kinase/genetics/metabolism ; Oligonucleotides, Antisense ; Phenotype ; Protein Kinase C/genetics/physiology ; Transcription Factors/genetics/physiology ; Zebrafish/*embryology/genetics ; Zebrafish Proteins/genetics/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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  • 9
    Publication Date: 2003-01-25
    Description: Disruption of the adaptor protein ELF, a beta-spectrin, leads to disruption of transforming growth factor-beta (TGF-beta) signaling by Smad proteins in mice. Elf-/- mice exhibit a phenotype similar to smad2+/-/smad3+/- mutant mice of midgestational death due to gastrointestinal, liver, neural, and heart defects. We show that TGF-beta triggers phosphorylation and association of ELF with Smad3 and Smad4, followed by nuclear translocation. ELF deficiency results in mislocalization of Smad3 and Smad4 and loss of the TGF-beta-dependent transcriptional response, which could be rescued by overexpression of the COOH-terminal region of ELF. This study reveals an unexpected molecular link between a major dynamic scaffolding protein and a key signaling pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tang, Yi -- Katuri, Varalakshmi -- Dillner, Allan -- Mishra, Bibhuti -- Deng, Chu-Xia -- Mishra, Lopa -- R01 DK56111/DK/NIDDK NIH HHS/ -- R01 DK58637/DK/NIDDK NIH HHS/ -- R03 DK53861/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2003 Jan 24;299(5606):574-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Developmental Biology, Department of Medicine, Georgetown University, Washington, DC 20007, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12543979" target="_blank"〉PubMed〈/a〉
    Keywords: Abnormalities, Multiple ; Animals ; Carrier Proteins/metabolism ; Cell Membrane/metabolism ; Cell Nucleus/metabolism ; Contractile Proteins/metabolism ; DNA-Binding Proteins/metabolism ; Embryonic and Fetal Development ; Filamins ; Gene Targeting ; Genes, fos ; Liver/abnormalities/embryology/*metabolism ; Mice ; Mice, Knockout ; Microfilament Proteins/metabolism ; Microscopy, Confocal ; Mutation ; Phenotype ; Phosphorylation ; Platelet-Derived Growth Factor/pharmacology ; *Signal Transduction ; Smad2 Protein ; Smad3 Protein ; Smad4 Protein ; Spectrin/genetics/*metabolism ; Trans-Activators/metabolism ; Transcriptional Activation ; Transforming Growth Factor beta/*metabolism/pharmacology ; 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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  • 10
    Publication Date: 2003-07-19
    Description: Mice in which all members of the Hox10 or Hox11 paralogous group are disrupted provide evidence that these Hox genes are involved in global patterning of the axial and appendicular skeleton. In the absence of Hox10 function, no lumbar vertebrae are formed. Instead, ribs project from all posterior vertebrae, extending caudally from the last thoracic vertebrae to beyond the sacral region. In the absence of Hox11 function, sacral vertebrae are not formed and instead these vertebrae assume a lumbar identity. The redundancy among these paralogous family members is so great that this global aspect of Hox patterning is not apparent in mice that are mutant for five of the six paralogous alleles.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wellik, Deneen M -- Capecchi, Mario R -- New York, N.Y. -- Science. 2003 Jul 18;301(5631):363-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and University of Utah, Salt Lake City, UT 84112, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12869760" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; *Body Patterning ; Bone and Bones/*embryology ; Female ; Forelimb/embryology ; Gene Expression Regulation, Developmental ; *Genes, Homeobox ; Hindlimb/embryology ; Homeodomain Proteins/*genetics/physiology ; Male ; Mice ; Mice, Mutant Strains ; Mutation ; Oncogene Proteins/*genetics/physiology ; Phenotype ; Spine/*embryology
    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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