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  • Phenotype  (31)
  • American Association for the Advancement of Science (AAAS)  (31)
  • American Association for the Advancement of Science
  • Oxford University Press
  • Springer Nature
  • 2000-2004  (31)
  • 1995-1999
  • 1980-1984
  • 1940-1944
  • 2002  (21)
  • 2000  (10)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (31)
  • American Association for the Advancement of Science
  • Oxford University Press
  • Springer Nature
  • Springer  (1)
Years
  • 2000-2004  (31)
  • 1995-1999
  • 1980-1984
  • 1940-1944
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  • 1
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    Comparative genome sequencing for discovery of novel polymorphisms in Bacillus anthracis (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-05-11
    Description: Comparison of the whole-genome sequence of Bacillus anthracis isolated from a victim of a recent bioterrorist anthrax attack with a reference reveals 60 new markers that include single nucleotide polymorphisms (SNPs), inserted or deleted sequences, and tandem repeats. Genome comparison detected four high-quality SNPs between the two sequenced B. anthracis chromosomes and seven differences among different preparations of the reference genome. These markers have been tested on a collection of anthrax isolates and were found to divide these samples into distinct families. These results demonstrate that genome-based analysis of microbial pathogens will provide a powerful new tool for investigation of infectious disease outbreaks.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Read, Timothy D -- Salzberg, Steven L -- Pop, Mihai -- Shumway, Martin -- Umayam, Lowell -- Jiang, Lingxia -- Holtzapple, Erik -- Busch, Joseph D -- Smith, Kimothy L -- Schupp, James M -- Solomon, Daniel -- Keim, Paul -- Fraser, Claire M -- R01-LM06845/LM/NLM NIH HHS/ -- New York, N.Y. -- Science. 2002 Jun 14;296(5575):2028-33. Epub 2002 May 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Institute for Genomic Research, 9712 Medical Center Drive, Rockville, MD 20850, USA., Department of Biological Sciences, Northern Arizona University, Flagstaff, AZ 86011, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12004073" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anthrax/microbiology ; Bacillus anthracis/classification/*genetics/isolation & ; purification/pathogenicity ; Bacterial Typing Techniques ; Base Sequence ; Bioterrorism ; Chromosome Inversion ; Computational Biology ; Disease Outbreaks ; Genetic Markers ; *Genetic Variation ; *Genome, Bacterial ; Genomics ; Humans ; Minisatellite Repeats ; Molecular Sequence Data ; Mutation ; Phenotype ; Phylogeny ; Plasmids ; *Polymorphism, Single Nucleotide ; Recombination, Genetic ; Repetitive Sequences, Nucleic Acid ; *Sequence Analysis, DNA ; Sequence Deletion ; Species Specificity ; Transposases/genetics ; Virulence/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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  • 2
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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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  • 3
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    Mitotic misregulation and human aging (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-03-31
    Description: Messenger RNA levels were measured in actively dividing fibroblasts isolated from young, middle-age, and old-age humans and humans with progeria, a rare genetic disorder characterized by accelerated aging. Genes whose expression is associated with age-related phenotypes and diseases were identified. The data also suggest that an underlying mechanism of the aging process involves increasing errors in the mitotic machinery of dividing cells in the postreproductive stage of life. We propose that this dysfunction leads to chromosomal pathologies that result in misregulation of genes involved in the aging process.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ly, D H -- Lockhart, D J -- Lerner, R A -- Schultz, P G -- New York, N.Y. -- Science. 2000 Mar 31;287(5462):2486-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and the Skaggs Institute for Chemical Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10741968" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Aged, 80 and over ; Aging/*genetics/pathology ; Biochemical Phenomena ; Cell Division ; Cell Line ; Cell Nucleus/ultrastructure ; Child ; Chromosome Segregation/genetics ; Disease/etiology ; Extracellular Matrix/metabolism ; Female ; Fibroblasts/cytology/*metabolism ; *Gene Expression Profiling ; *Gene Expression Regulation ; Humans ; Male ; Middle Aged ; *Mitosis/genetics ; Mutation ; Oligonucleotide Array Sequence Analysis ; Phenotype ; Progeria/*genetics/pathology ; RNA, Messenger/genetics/metabolism ; Spindle Apparatus/metabolism ; Transcription Factors/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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    Sustained loss of a neoplastic phenotype by brief inactivation of MYC (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-07-06
    Description: Pharmacological inactivation of oncogenes is being investigated as a possible therapeutic strategy for cancer. One potential drawback is that cessation of such therapy may allow reactivation of the oncogene and tumor regrowth. We used a conditional transgenic mouse model for MYC-induced tumorigenesis to demonstrate that brief inactivation of MYC results in the sustained regression of tumors and the differentiation of osteogenic sarcoma cells into mature osteocytes. Subsequent reactivation of MYC did not restore the cells' malignant properties but instead induced apoptosis. Thus, brief MYC inactivation appears to cause epigenetic changes in tumor cells that render them insensitive to MYC-induced tumorigenesis. These results raise the possibility that transient inactivation of MYC may be an effective therapy for certain cancers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jain, Meenakshi -- Arvanitis, Constadina -- Chu, Kenneth -- Dewey, William -- Leonhardt, Edith -- Trinh, Maxine -- Sundberg, Christopher D -- Bishop, J Michael -- Felsher, Dean W -- K08-CA75967-01/CA/NCI NIH HHS/ -- R01-CA85610/CA/NCI NIH HHS/ -- R01-CA89305-01/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2002 Jul 5;297(5578):102-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Oncology, Departments of Medicine and Pathology, Stanford University, Stanford, CA 94305-5151, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12098700" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/administration & dosage/therapeutic use ; Apoptosis ; Cell Differentiation ; Cell Division ; Doxycycline/pharmacology ; Gene Expression/drug effects ; *Gene Silencing ; *Genes, myc ; Mice ; Mice, Transgenic ; Neoplasm Transplantation ; Osteocytes/cytology ; Osteosarcoma/drug therapy/*genetics/*pathology ; Phenotype ; Transgenes ; 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 conserved p38 MAP kinase pathway in Caenorhabditis elegans innate immunity (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-07-27
    Description: A genetic screen for Caenorhabditis elegans mutants with enhanced susceptibility to killing by Pseudomonas aeruginosa led to the identification of two genes required for pathogen resistance: sek-1, which encodes a mitogen-activated protein (MAP) kinase kinase, and nsy-1, which encodes a MAP kinase kinase kinase. RNA interference assays and biochemical analysis established that a p38 ortholog, pmk-1, functions as the downstream MAP kinase required for pathogen defense. These data suggest that this MAP kinase signaling cassette represents an ancient feature of innate immune responses in evolutionarily diverse species.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Dennis H -- Feinbaum, Rhonda -- Alloing, Genevieve -- Emerson, Fred E -- Garsin, Danielle A -- Inoue, Hideki -- Tanaka-Hino, Miho -- Hisamoto, Naoki -- Matsumoto, Kunihiro -- Tan, Man-Wah -- Ausubel, Frederick M -- GM48707/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2002 Jul 26;297(5581):623-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12142542" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/*enzymology/genetics/*immunology/microbiology ; Caenorhabditis elegans Proteins/genetics/*metabolism ; Genes, Helminth ; *Immunity, Innate ; *MAP Kinase Signaling System ; Mitogen-Activated Protein Kinase Kinases/genetics/metabolism ; Mitogen-Activated Protein Kinases/genetics/*metabolism ; Mutation ; Phenotype ; Pseudomonas aeruginosa/*immunology/physiology ; p38 Mitogen-Activated Protein Kinases
    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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    Genetic loci affecting resistance to human malaria parasites in a West African mosquito vector population (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-10-05
    Description: Successful propagation of the malaria parasite Plasmodium falciparum within a susceptible mosquito vector is a prerequisite for the transmission of malaria. A field-based genetic analysis of the major human malaria vector, Anopheles gambiae, has revealed natural factors that reduce the transmission of P. falciparum. Differences in P. falciparum oocyst numbers between mosquito isofemale families fed on the same infected blood indicated a large genetic component affecting resistance to the parasite, and genome-wide scanning in pedigrees of wild mosquitoes detected segregating resistance alleles. The apparently high natural frequency of resistance alleles suggests that malaria parasites (or a similar pathogen) exert a significant selective pressure on vector populations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Niare, Oumou -- Markianos, Kyriacos -- Volz, Jennifer -- Oduol, Frederick -- Toure, Abdoulaye -- Bagayoko, Magaran -- Sangare, Djibril -- Traore, Sekou F -- Wang, Rui -- Blass, Claudia -- Dolo, Guimogo -- Bouare, Madama -- Kafatos, Fotis C -- Kruglyak, Leonid -- Toure, Yeya T -- Vernick, Kenneth D -- New York, N.Y. -- Science. 2002 Oct 4;298(5591):213-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical and Molecular Parasitology, New York University School of Medicine, 341 East 25th Street, New York, NY 10010, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12364806" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Anopheles/*genetics/immunology/*parasitology/physiology ; Chromosome Mapping ; Female ; *Genes, Insect ; Genetic Linkage ; Genetic Markers ; Genome ; Genotype ; Host-Parasite Interactions ; Humans ; Insect Vectors/genetics/immunology/*parasitology/physiology ; Karyotyping ; Malaria, Falciparum/transmission ; Male ; Mali ; Oviposition ; Phenotype ; Plasmodium falciparum/pathogenicity/*physiology ; Virulence
    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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    Chloroquine resistance in Plasmodium falciparum malaria parasites conferred by pfcrt mutations (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-10-05
    Description: Plasmodium falciparum chloroquine resistance is a major cause of worldwide increases in malaria mortality and morbidity. Recent laboratory and clinical studies have associated chloroquine resistance with point mutations in the gene pfcrt. However, direct proof of a causal relationship has remained elusive and most models have posited a multigenic basis of resistance. Here, we provide conclusive evidence that mutant haplotypes of the pfcrt gene product of Asian, African, or South American origin confer chloroquine resistance with characteristic verapamil reversibility and reduced chloroquine accumulation. pfcrt mutations increased susceptibility to artemisinin and quinine and minimally affected amodiaquine activity; hence, these antimalarials warrant further investigation as agents to control chloroquine-resistant falciparum malaria.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2954758/" 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/PMC2954758/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sidhu, Amar Bir Singh -- Verdier-Pinard, Dominik -- Fidock, David A -- R01 AI050234/AI/NIAID NIH HHS/ -- R01 AI050234-03/AI/NIAID NIH HHS/ -- R01 AI50234/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2002 Oct 4;298(5591):210-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12364805" target="_blank"〉PubMed〈/a〉
    Keywords: *ATP-Binding Cassette Transporters ; Alleles ; Amodiaquine/pharmacology ; Animals ; Antimalarials/metabolism/*pharmacology ; *Artemisinins ; Chloroquine/metabolism/*pharmacology ; Cloning, Molecular ; Drug Resistance/*genetics ; Genes, Protozoan ; Haplotypes ; Mefloquine/pharmacology ; Membrane Proteins/*genetics/physiology ; Membrane Transport Proteins ; Parasitic Sensitivity Tests ; Phenotype ; Plasmodium falciparum/*drug effects/genetics/metabolism ; *Point Mutation ; Protozoan Proteins/genetics/physiology ; Quinine/pharmacology ; Sesquiterpenes/pharmacology ; Transfection ; Verapamil/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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  • 8
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    Inhibition of excess nodal signaling during mouse gastrulation by the transcriptional corepressor DRAP1 (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-12-10
    Description: The formation and patterning of mesoderm during mammalian gastrulation require the activity of Nodal, a secreted mesoderm-inducing factor of the transforming growth factor-beta (TGF-beta) family. Here we show that the transcriptional corepressor DRAP1 has a very specific role in regulation of Nodal activity during mouse embryogenesis. We find that loss of Drap1 leads to severe gastrulation defects that are consistent with increased expression of Nodal and can be partially suppressed by Nodal heterozygosity. Biochemical studies indicate that DRAP1 interacts with and inhibits DNA binding by the winged-helix transcription factor FoxH1 (FAST), a critical component of a positive feedback loop for Nodal activity. We propose that DRAP1 limits the spread of a morphogenetic signal by down-modulating the response to the Nodal autoregulatory loop.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Iratni, Rabah -- Yan, Yu-Ting -- Chen, Canhe -- Ding, Jixiang -- Zhang, Yi -- Price, Sandy M -- Reinberg, Danny -- Shen, Michael M -- New York, N.Y. -- Science. 2002 Dec 6;298(5600):1996-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Biochemistry, Division of Nucleic Acids Enzymology, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, Piscataway, NJ 08854, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12471260" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Cell Line ; Crosses, Genetic ; DNA/metabolism ; DNA-Binding Proteins/metabolism ; *Embryonic and Fetal Development ; Female ; Forkhead Transcription Factors ; Gastrula/*physiology ; Gene Expression Regulation, Developmental ; Gene Targeting ; Heterozygote ; In Situ Hybridization ; Left-Right Determination Factors ; Male ; Mesoderm/cytology/physiology ; Mice ; Morphogenesis ; Mutation ; Nodal Protein ; Phenotype ; Protein Binding ; RNA Interference ; Recombinant Fusion Proteins/metabolism ; Repressor Proteins/genetics/*metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; *Signal Transduction ; Transcription Factors/metabolism ; Transforming Growth Factor beta/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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  • 9
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    A tomato cysteine protease required for Cf-2-dependent disease resistance and suppression of autonecrosis (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-04-27
    Description: Little is known of how plant disease resistance (R) proteins recognize pathogens and activate plant defenses. Rcr3 is specifically required for the function of Cf-2, a Lycopersicon pimpinellifolium gene bred into cultivated tomato (Lycopersicon esculentum) for resistance to Cladosporium fulvum. Rcr3 encodes a secreted papain-like cysteine endoprotease. Genetic analysis shows Rcr3 is allelic to the L. pimpinellifolium Ne gene, which suppresses the Cf-2-dependent autonecrosis conditioned by its L. esculentum allele, ne (necrosis). Rcr3 alleles from these two species encode proteins that differ by only seven amino acids. Possible roles of Rcr3 in Cf-2-dependent defense and autonecrosis are discussed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kruger, Julia -- Thomas, Colwyn M -- Golstein, Catherine -- Dixon, Mark S -- Smoker, Matthew -- Tang, Saijun -- Mulder, Lonneke -- Jones, Jonathan D G -- New York, N.Y. -- Science. 2002 Apr 26;296(5568):744-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Sainsbury Laboratory, John Innes Centre, Norwich NR4 7UH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11976458" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Sequence ; Base Sequence ; Cladosporium/*physiology ; Cloning, Molecular ; Cysteine Endopeptidases/chemistry/*genetics/*metabolism ; Cysteine Proteinase Inhibitors/pharmacology ; Gene Expression Regulation, Plant ; *Genes, Plant ; Immunity, Innate ; Leucine/analogs & derivatives/pharmacology ; Lycopersicon esculentum/*enzymology/genetics/*microbiology/physiology ; Molecular Sequence Data ; Mutation ; Phenotype ; *Plant Diseases ; Plant Leaves/enzymology ; Plant Proteins/*metabolism ; Plants, Genetically Modified ; Promoter Regions, Genetic ; Recombinant Fusion Proteins/chemistry/metabolism ; Tobacco/genetics ; Transgenes
    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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    A low genomic number of recessive lethals in natural populations of bluefin killifish and zebrafish (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-06-29
    Description: Despite the importance of selection against deleterious mutations in natural populations, reliable estimates of the genomic numbers of mutant alleles in wild populations are scarce. We found that, in wild-caught bluefin killifish Lucania goodei (Fundulidae) and wild-caught zebrafish Danio rerio (Cyprinidae), the average numbers of recessive lethal alleles per individual are 1.9 (95% confidence limits 1.3 to 2.6) and 1.4 (95% confidence limits 1.0 to 2.0), respectively. These results, together with data on several Drosophila species and on Xenopus laevis, show that phylogenetically distant animals with different genome sizes and numbers of genes carry similar numbers of lethal mutations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McCune, Amy R -- Fuller, Rebecca C -- Aquilina, Allisan A -- Dawley, Robert M -- Fadool, James M -- Houle, David -- Travis, Joseph -- Kondrashov, Alexey S -- New York, N.Y. -- Science. 2002 Jun 28;296(5577):2398-401.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ecology and Evolutionary Biology, Cornell University, Ithaca, NY 14853, USA. arm2@cornell.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12089444" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Crosses, Genetic ; Drosophila/genetics ; Female ; Fundulidae/abnormalities/*genetics ; *Genes, Lethal ; *Genes, Recessive ; *Genome ; Likelihood Functions ; Male ; Mutation ; Phenotype ; Xenopus laevis/genetics ; Zebrafish/abnormalities/*genetics
    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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