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  • Transcription, Genetic  (327)
  • American Association for the Advancement of Science (AAAS)  (327)
  • American Chemical Society (ACS)
  • National Academy of Sciences
  • PANGAEA
  • 2005-2009  (176)
  • 1985-1989  (151)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (327)
  • American Chemical Society (ACS)
  • National Academy of Sciences
  • PANGAEA
  • Nature Publishing Group (NPG)  (22)
Years
Year
  • 1
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    RNAi in budding yeast (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-09-12
    Description: RNA interference (RNAi), a gene-silencing pathway triggered by double-stranded RNA, is conserved in diverse eukaryotic species but has been lost in the model budding yeast Saccharomyces cerevisiae. Here, we show that RNAi is present in other budding yeast species, including Saccharomyces castellii and Candida albicans. These species use noncanonical Dicer proteins to generate small interfering RNAs, which mostly correspond to transposable elements and Y' subtelomeric repeats. In S. castellii, RNAi mutants are viable but have excess Y' messenger RNA levels. In S. cerevisiae, introducing Dicer and Argonaute of S. castellii restores RNAi, and the reconstituted pathway silences endogenous retrotransposons. These results identify a previously unknown class of Dicer proteins, bring the tool of RNAi to the study of budding yeasts, and bring the tools of budding yeast to the study of RNAi.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3786161/" 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/PMC3786161/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Drinnenberg, Ines A -- Weinberg, David E -- Xie, Kathleen T -- Mower, Jeffrey P -- Wolfe, Kenneth H -- Fink, Gerald R -- Bartel, David P -- GM0305010/GM/NIGMS NIH HHS/ -- GM040266/GM/NIGMS NIH HHS/ -- GM067031/GM/NIGMS NIH HHS/ -- R01 GM067031/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Oct 23;326(5952):544-50. doi: 10.1126/science.1176945. Epub 2009 Sep 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, 9 Cambridge Center, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19745116" target="_blank"〉PubMed〈/a〉
    Keywords: Fungal Proteins/genetics/metabolism ; Gene Expression Profiling ; Genes, Fungal ; Genetic Loci ; Mutation ; Open Reading Frames ; *RNA Interference ; RNA, Double-Stranded/genetics/metabolism ; RNA, Fungal/genetics/metabolism ; RNA, Messenger/genetics/metabolism ; RNA, Small Interfering/genetics/*metabolism ; Repetitive Sequences, Nucleic Acid ; Retroelements ; Ribonuclease III/genetics/metabolism ; Saccharomyces/*genetics/metabolism ; Saccharomyces cerevisiae/*genetics/metabolism ; Saccharomyces cerevisiae Proteins/genetics/metabolism ; Saccharomycetales/*genetics/metabolism ; Sequence Analysis, RNA ; Transcription, Genetic ; Transformation, Genetic
    Print ISSN: 0036-8075
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  • 2
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    Circadian rhythms. Linking the loops (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McClung, C Robertson -- New York, N.Y. -- Science. 2009 Mar 13;323(5920):1440-1. doi: 10.1126/science.1171418.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Dartmouth College, Hanover, NH 03755, USA. c.robertson.mcclung@dartmouth.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19286545" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/genetics/*physiology ; Arabidopsis Proteins/genetics/*metabolism ; Biological Clocks/*genetics ; Circadian Rhythm/*genetics ; DNA-Binding Proteins/genetics/metabolism ; Feedback, Physiological ; *Gene Expression Regulation, Plant ; Genes, Plant ; Promoter Regions, Genetic ; Repressor Proteins/genetics/*metabolism ; Transcription Factors/genetics/*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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  • 3
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    RNA polymerase IV functions in paramutation in Zea mays (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-03
    Description: Plants have distinct RNA polymerase complexes (Pol IV and Pol V) with largely unknown roles in maintaining small RNA-associated gene silencing. Curiously, the eudicot Arabidopsis thaliana is not affected when either function is lost. By use of mutation selection and positional cloning, we showed that the largest subunit of the presumed maize Pol IV is involved in paramutation, an inherited epigenetic change facilitated by an interaction between two alleles, as well as normal maize development. Bioinformatics analyses and nuclear run-on transcription assays indicate that Pol IV does not engage in the efficient RNA synthesis typical of the three major eukaryotic DNA-dependent RNA polymerases. These results indicate that Pol IV employs abnormal RNA polymerase activities to achieve genome-wide silencing and that its absence affects both maize development and heritable epigenetic changes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Erhard, Karl F Jr -- Stonaker, Jennifer L -- Parkinson, Susan E -- Lim, Jana P -- Hale, Christopher J -- Hollick, Jay B -- New York, N.Y. -- Science. 2009 Feb 27;323(5918):1201-5. doi: 10.1126/science.1164508.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Plant and Microbial Biology, 111 Koshland Hall, University of California, Berkeley, CA 94720-3102, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19251626" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Sequence ; Base Sequence ; Computational Biology ; DNA-Directed RNA Polymerases/chemistry/genetics/*metabolism ; *Epigenesis, Genetic ; Gene Silencing ; Genes, Plant ; Molecular Sequence Data ; *Mutation ; Phylogeny ; Protein Subunits/chemistry/genetics/metabolism ; RNA, Plant/genetics/metabolism ; RNA, Small Interfering/genetics/metabolism ; Transcription, Genetic ; Zea mays/*enzymology/*genetics/growth & development
    Print ISSN: 0036-8075
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  • 4
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    Reversal of RNA dominance by displacement of protein sequestered on triplet repeat RNA (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-07-18
    Description: Genomic expansions of simple tandem repeats can give rise to toxic RNAs that contain expanded repeats. In myotonic dystrophy, the expression of expanded CUG repeats (CUGexp) causes abnormal regulation of alternative splicing and neuromuscular dysfunction. We used a transgenic mouse model to show that derangements of myotonic dystrophy are reversed by a morpholino antisense oligonucleotide, CAG25, that binds to CUGexp RNA and blocks its interaction with muscleblind-like 1 (MBNL1), a CUGexp-binding protein. CAG25 disperses nuclear foci of CUGexp RNA and reduces the overall burden of this toxic RNA. As MBNL1 is released from sequestration, the defect of alternative splicing regulation is corrected, thereby restoring ion channel function. These findings suggest an alternative use of antisense methods, to inhibit deleterious interactions of proteins with pathogenic RNAs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4109973/" 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/PMC4109973/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wheeler, Thurman M -- Sobczak, Krzysztof -- Lueck, John D -- Osborne, Robert J -- Lin, Xiaoyan -- Dirksen, Robert T -- Thornton, Charles A -- AR/NS48143/AR/NIAMS NIH HHS/ -- AR046806/AR/NIAMS NIH HHS/ -- K08 NS064293/NS/NINDS NIH HHS/ -- K24 AR048143/AR/NIAMS NIH HHS/ -- NIDCR-T32DE07202/DE/NIDCR NIH HHS/ -- R01 AR046806/AR/NIAMS NIH HHS/ -- R01 AR049077/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2009 Jul 17;325(5938):336-9. doi: 10.1126/science.1173110.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Neurology, Pharmacology and Physiology, University of Rochester, Rochester, NY 14642, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19608921" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions/genetics/*metabolism ; Actins/genetics ; Alternative Splicing ; Animals ; Cell Line ; Cell Nucleus/metabolism ; Chloride Channels/metabolism ; DNA-Binding Proteins/*metabolism ; Humans ; Mice ; Mice, Knockout ; Mice, Transgenic ; Myotonic Dystrophy/*drug therapy/*genetics/metabolism ; Myotonin-Protein Kinase ; Oligodeoxyribonucleotides, Antisense/*pharmacology/therapeutic use ; Protein-Serine-Threonine Kinases/genetics ; RNA, Messenger/genetics ; RNA-Binding Proteins/*metabolism ; Transcription, Genetic ; *Trinucleotide Repeat Expansion
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 5
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    Paternal control of embryonic patterning in Arabidopsis thaliana (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-17
    Description: The YODA (YDA) mitogen-activated protein kinase pathway promotes elongation of the Arabidopsis zygote and development of its basal daughter cell into the extra-embryonic suspensor. Here, we show that the interleukin-1 receptor-associated kinase (IRAK)/Pelle-like kinase gene SHORT SUSPENSOR (SSP) regulates this pathway through a previously unknown parent-of-origin effect. SSP transcripts are produced in mature pollen but do not appear to be translated. Instead, they are delivered via the sperm cells to the zygote and the endosperm, where SSP protein transiently accumulates. Ectopic expression of SSP protein in the leaf epidermis is sufficient to activate YDA-dependent signaling. We propose that SSP protein produced from paternal transcripts upon fertilization triggers zygotic YDA activity, providing an essential temporal cue for the regulation of the asymmetric first division.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bayer, Martin -- Nawy, Tal -- Giglione, Carmela -- Galli, Mary -- Meinnel, Thierry -- Lukowitz, Wolfgang -- New York, N.Y. -- Science. 2009 Mar 13;323(5920):1485-8. doi: 10.1126/science.1167784.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19286558" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Arabidopsis/*embryology/*genetics/metabolism ; Arabidopsis Proteins/*metabolism ; Biocatalysis ; Catalytic Domain ; Cell Division ; Crosses, Genetic ; *Gene Expression Regulation, Plant ; Genomic Imprinting ; Interleukin-1 Receptor-Associated Kinases/chemistry/*genetics/*metabolism ; MAP Kinase Kinase Kinases/*metabolism ; MAP Kinase Signaling System ; Mutation ; Plants, Genetically Modified ; Pollen/metabolism ; Protein Binding ; Protein Structure, Tertiary ; RNA, Messenger/genetics/metabolism ; Recombinant Fusion Proteins ; Seeds/growth & development/metabolism ; Transcription, Genetic
    Print ISSN: 0036-8075
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  • 6
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    A frazzled/DCC-dependent transcriptional switch regulates midline axon guidance (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-28
    Description: Precise wiring of the nervous system depends on coordinating the action of conserved families of proteins that direct axons to their appropriate targets. Slit-roundabout repulsion and netrin-deleted in colorectal cancer (DCC) (frazzled) attraction must be tightly regulated to control midline axon guidance in vertebrates and invertebrates, but the mechanism mediating this regulation is poorly defined. Here, we show that the Fra receptor has two genetically separable functions in regulating midline guidance in Drosophila. First, Fra mediates canonical chemoattraction in response to netrin, and, second, it functions independently of netrin to activate commissureless transcription, allowing attraction to be coupled to the down-regulation of repulsion in precrossing commissural axons.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4078765/" 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/PMC4078765/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, Long -- Garbe, David S -- Bashaw, Greg J -- NS046333/NS/NINDS NIH HHS/ -- NS054739/NS/NINDS NIH HHS/ -- R01 NS046333/NS/NINDS NIH HHS/ -- R01 NS046333-07/NS/NINDS NIH HHS/ -- R01 NS054739/NS/NINDS NIH HHS/ -- R01 NS054739-03/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2009 May 15;324(5929):944-7. doi: 10.1126/science.1171320. Epub 2009 Mar 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, University of Pennsylvania School of Medicine, 1113 BRB2/3, 421 Curie Boulevard, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19325078" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology ; Drosophila Proteins/*genetics/metabolism ; Drosophila melanogaster/embryology/*genetics/metabolism ; *Gene Expression Regulation, Developmental ; Membrane Proteins/*genetics/metabolism ; Mutation ; Nerve Growth Factors/metabolism ; Nerve Tissue Proteins/genetics/metabolism ; Nervous System/embryology/growth & development ; Neurons/*physiology ; RNA, Messenger/genetics/metabolism ; Receptors, Cell Surface/genetics/*metabolism ; Receptors, Immunologic/genetics ; Signal Transduction ; Transcription, Genetic ; *Transcriptional Activation
    Print ISSN: 0036-8075
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  • 7
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    Circadian rhythms. A circadian loop asSIRTs itself (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wijnen, Herman -- R01 GM078339/GM/NIGMS NIH HHS/ -- R01 GM078339-03/GM/NIGMS NIH HHS/ -- R01 GM78839/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2009 May 1;324(5927):598-9. doi: 10.1126/science.1174132.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of Virginia, Charlottesville, VA 22904, USA. hw9u@virginai.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19407188" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors ; Acetylation ; Acrylamides/pharmacology ; Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics/metabolism ; *Biological Clocks ; CLOCK Proteins ; *Circadian Rhythm ; Cytokines/antagonists & inhibitors/genetics/*metabolism ; *Feedback, Physiological ; Gene Expression Regulation ; Mice ; Mutation ; NAD/*metabolism ; Nicotinamide Phosphoribosyltransferase/antagonists & ; inhibitors/genetics/*metabolism ; Piperidines/pharmacology ; Sirtuin 1 ; Sirtuins/*metabolism ; Trans-Activators/genetics/metabolism ; Transcription Factors/genetics/metabolism ; Transcription, Genetic
    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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  • 8
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    Impact of genome reduction on bacterial metabolism and its regulation (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-08
    Description: To understand basic principles of bacterial metabolism organization and regulation, but also the impact of genome size, we systematically studied one of the smallest bacteria, Mycoplasma pneumoniae. A manually curated metabolic network of 189 reactions catalyzed by 129 enzymes allowed the design of a defined, minimal medium with 19 essential nutrients. More than 1300 growth curves were recorded in the presence of various nutrient concentrations. Measurements of biomass indicators, metabolites, and 13C-glucose experiments provided information on directionality, fluxes, and energetics; integration with transcription profiling enabled the global analysis of metabolic regulation. Compared with more complex bacteria, the M. pneumoniae metabolic network has a more linear topology and contains a higher fraction of multifunctional enzymes; general features such as metabolite concentrations, cellular energetics, adaptability, and global gene expression responses are similar, however.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yus, Eva -- Maier, Tobias -- Michalodimitrakis, Konstantinos -- van Noort, Vera -- Yamada, Takuji -- Chen, Wei-Hua -- Wodke, Judith A H -- Guell, Marc -- Martinez, Sira -- Bourgeois, Ronan -- Kuhner, Sebastian -- Raineri, Emanuele -- Letunic, Ivica -- Kalinina, Olga V -- Rode, Michaela -- Herrmann, Richard -- Gutierrez-Gallego, Ricardo -- Russell, Robert B -- Gavin, Anne-Claude -- Bork, Peer -- Serrano, Luis -- New York, N.Y. -- Science. 2009 Nov 27;326(5957):1263-8. doi: 10.1126/science.1177263.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Genomic Regulation (CRG) and Universitat Pompeu Fabra, Avenida Dr. Aiguader 88, 08003 Barcelona, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965476" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Bacterial Proteins/*metabolism ; Culture Media ; Energy Metabolism ; Enzymes/genetics/metabolism ; Gene Expression Profiling ; *Gene Expression Regulation, Bacterial ; *Genome, Bacterial ; Glycolysis ; *Metabolic Networks and Pathways ; Mycoplasma pneumoniae/*genetics/growth & development/*metabolism ; RNA, Bacterial/genetics/metabolism ; Signal Transduction ; Systems Biology ; Transcription, Genetic ; rRNA Operon
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  • 9
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    Genetics. More than just a copy (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-08-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaessmann, Henrik -- New York, N.Y. -- Science. 2009 Aug 21;325(5943):958-9. doi: 10.1126/science.1178487.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Integrative Genomics, University of Lausanne, Genopode Building, CH-1015 Lausanne, Switzerland. henrik.kaessmann@unil.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19696341" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chondrocytes/metabolism ; Dogs/anatomy & histology/embryology/*genetics ; Evolution, Molecular ; Extremities/*anatomy & histology/embryology ; Fibroblast Growth Factor 4/*genetics ; *Gene Duplication ; Gene Expression Regulation ; *Genes, Duplicate ; Humerus/embryology/metabolism ; Long Interspersed Nucleotide Elements ; Promoter Regions, Genetic ; Regulatory Sequences, Nucleic Acid ; Retroelements ; Selection, Genetic ; Species Specificity ; Transcription, Genetic
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  • 10
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    Synthetic heterochromatin bypasses RNAi and centromeric repeats to establish functional centromeres (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-06-27
    Description: In the central domain of fission yeast centromeres, the kinetochore is assembled on CENP-A(Cnp1) nucleosomes. Normally, small interfering RNAs generated from flanking outer repeat transcripts direct histone H3 lysine 9 methyltransferase Clr4 to homologous loci to form heterochromatin. Outer repeats, RNA interference (RNAi), and centromeric heterochromatin are required to establish CENP-A(Cnp1) chromatin. We demonstrated that tethering Clr4 via DNA-binding sites at euchromatic loci induces heterochromatin assembly, with or without active RNAi. This synthetic heterochromatin completely substitutes for outer repeats on plasmid-based minichromosomes, promoting de novo CENP-A(Cnp1) and kinetochore assembly, to allow their mitotic segregation, even with RNAi inactive. Thus, the role of outer repeats in centromere establishment is simply the provision of RNAi substrates to direct heterochromatin formation; H3K9 methylation-dependent heterochromatin is alone sufficient to form functional centromeres.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2949999/" 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/PMC2949999/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kagansky, Alexander -- Folco, Hernan Diego -- Almeida, Ricardo -- Pidoux, Alison L -- Boukaba, Abdelhalim -- Simmer, Femke -- Urano, Takeshi -- Hamilton, Georgina L -- Allshire, Robin C -- 065061/Wellcome Trust/United Kingdom -- 065061/Z/Wellcome Trust/United Kingdom -- G0301153/Medical Research Council/United Kingdom -- G0301153(69173)/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2009 Jun 26;324(5935):1716-9. doi: 10.1126/science.1172026.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Centre for Cell Biology, School of Biological Sciences, The University of Edinburgh, 6.34 Swann Building, Edinburgh EH9 3JR, Scotland, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19556509" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites ; Cell Cycle Proteins/metabolism ; Centromere/chemistry/*metabolism/ultrastructure ; *Chromatin Assembly and Disassembly ; Chromosomal Proteins, Non-Histone/metabolism ; Chromosome Segregation ; DNA-Binding Proteins/genetics/metabolism ; Heterochromatin/*metabolism ; Histones/metabolism ; Kinetochores/metabolism ; Methyltransferases/metabolism ; Mitosis ; *RNA Interference ; Recombinant Fusion Proteins/metabolism ; Saccharomyces cerevisiae Proteins/genetics/metabolism ; Schizosaccharomyces/genetics/*metabolism ; Schizosaccharomyces pombe Proteins/metabolism ; Transcription Factors/genetics/metabolism ; Transcription, Genetic
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  • 11
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    KLF family members regulate intrinsic axon regeneration ability (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-10-10
    Description: Neurons in the central nervous system (CNS) lose their ability to regenerate early in development, but the underlying mechanisms are unknown. By screening genes developmentally regulated in retinal ganglion cells (RGCs), we identified Kruppel-like factor-4 (KLF4) as a transcriptional repressor of axon growth in RGCs and other CNS neurons. RGCs lacking KLF4 showed increased axon growth both in vitro and after optic nerve injury in vivo. Related KLF family members suppressed or enhanced axon growth to differing extents, and several growth-suppressive KLFs were up-regulated postnatally, whereas growth-enhancing KLFs were down-regulated. Thus, coordinated activities of different KLFs regulate the regenerative capacity of CNS neurons.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2882032/" 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/PMC2882032/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moore, Darcie L -- Blackmore, Murray G -- Hu, Ying -- Kaestner, Klaus H -- Bixby, John L -- Lemmon, Vance P -- Goldberg, Jeffrey L -- P30 EY014801/EY/NEI NIH HHS/ -- R01 NS059866/NS/NINDS NIH HHS/ -- R01 NS059866-01A2/NS/NINDS NIH HHS/ -- R01 NS061348/NS/NINDS NIH HHS/ -- R01 NS061348-01A2/NS/NINDS NIH HHS/ -- R01 NS061348-02/NS/NINDS NIH HHS/ -- R01 NS061348-03/NS/NINDS NIH HHS/ -- R01 NS061348-04/NS/NINDS NIH HHS/ -- R03 EY016790/EY/NEI NIH HHS/ -- R03 EY016790-01/EY/NEI NIH HHS/ -- R03 EY016790-02/EY/NEI NIH HHS/ -- R03 EY016790-03/EY/NEI NIH HHS/ -- T32 NS007459/NS/NINDS NIH HHS/ -- T32 NS07492/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2009 Oct 9;326(5950):298-301. doi: 10.1126/science.1175737.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Bascom Palmer Eye Institute, University of Miami Miller School of Medicine, Miami, FL 33136, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19815778" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology/ultrastructure ; Cell Count ; Cell Survival ; Cells, Cultured ; Down-Regulation ; Gene Knockout Techniques ; Growth Cones/physiology ; Hippocampus/cytology/physiology ; Kruppel-Like Transcription Factors/genetics/*physiology ; Mice ; Nerve Crush ; Nerve Regeneration ; Neurites/physiology ; Neurons/*physiology ; Optic Nerve Injuries/physiopathology ; Rats ; Retinal Ganglion Cells/cytology/*physiology ; Transcription, Genetic ; Transfection ; Up-Regulation
    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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  • 12
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    Biochemistry. Nascent proteins caught in the act (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kampmann, Martin -- Blobel, Gunter -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Dec 4;326(5958):1352-3. doi: 10.1126/science.1183690.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and The Rockefeller University, New York, NY 10065, USA. martin.kampmann@rockefeller.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965743" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites ; Cryoelectron Microscopy ; Endoplasmic Reticulum/metabolism/ultrastructure ; Escherichia coli Proteins/chemistry/genetics/*metabolism/ultrastructure ; Gene Expression Regulation, Bacterial ; Membrane Proteins/chemistry/*metabolism/ultrastructure ; Operon ; Protein Biosynthesis ; Protein Multimerization ; Protein Sorting Signals ; Protein Transport ; Proteins/chemistry/*metabolism/ultrastructure ; RNA, Transfer/metabolism ; Ribosomes/*metabolism/ultrastructure ; Signal Recognition Particle/chemistry/metabolism/ultrastructure ; Transcription, Genetic ; Tryptophanase/chemistry/*genetics/metabolism
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  • 13
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    Analysis of Drosophila segmentation network identifies a JNK pathway factor overexpressed in kidney cancer (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-01-24
    Description: We constructed a large-scale functional network model in Drosophila melanogaster built around two key transcription factors involved in the process of embryonic segmentation. Analysis of the model allowed the identification of a new role for the ubiquitin E3 ligase complex factor SPOP. In Drosophila, the gene encoding SPOP is a target of segmentation transcription factors. Drosophila SPOP mediates degradation of the Jun kinase phosphatase Puckered, thereby inducing tumor necrosis factor (TNF)/Eiger-dependent apoptosis. In humans, we found that SPOP plays a conserved role in TNF-mediated JNK signaling and was highly expressed in 99% of clear cell renal cell carcinomas (RCCs), the most prevalent form of kidney cancer. SPOP expression distinguished histological subtypes of RCC and facilitated identification of clear cell RCC as the primary tumor for metastatic lesions.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2756524/" 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/PMC2756524/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Jiang -- Ghanim, Murad -- Xue, Lei -- Brown, Christopher D -- Iossifov, Ivan -- Angeletti, Cesar -- Hua, Sujun -- Negre, Nicolas -- Ludwig, Michael -- Stricker, Thomas -- Al-Ahmadie, Hikmat A -- Tretiakova, Maria -- Camp, Robert L -- Perera-Alberto, Montse -- Rimm, David L -- Xu, Tian -- Rzhetsky, Andrey -- White, Kevin P -- P50 GM081892/GM/NIGMS NIH HHS/ -- P50 GM081892-01A1/GM/NIGMS NIH HHS/ -- R01 HG003012/HG/NHGRI NIH HHS/ -- R01 HG003012-04/HG/NHGRI NIH HHS/ -- UL1 RR024999/RR/NCRR NIH HHS/ -- UL1 RR024999-02/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2009 Feb 27;323(5918):1218-22. doi: 10.1126/science.1157669. Epub 2009 Jan 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Genomics and Systems Biology, University of Chicago and Argonne National Laboratory, Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19164706" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Apoptosis ; Carcinoma, Renal Cell/*genetics/metabolism ; Cell Line ; Compound Eye, Arthropod/embryology/metabolism ; Drosophila Proteins/genetics/metabolism ; Drosophila melanogaster/embryology/*genetics/metabolism ; Embryo, Nonmammalian/metabolism ; Fushi Tarazu Transcription Factors/genetics/metabolism ; Gene Expression Profiling ; Gene Regulatory Networks ; Homeodomain Proteins/genetics/metabolism ; Humans ; Janus Kinases/*metabolism ; Kidney/metabolism ; Kidney Neoplasms/*genetics/metabolism ; Molecular Sequence Data ; Nervous System/embryology ; Nuclear Proteins/*genetics/metabolism ; Phosphoprotein Phosphatases/metabolism ; Phosphorylation ; Repressor Proteins/*genetics/metabolism ; *Signal Transduction ; Transcription Factors/genetics/metabolism ; Transcription, Genetic
    Print ISSN: 0036-8075
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  • 14
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    The increasing complexity of the cancer stem cell paradigm (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-06-27
    Description: The investigation and study of cancer stem cells (CSCs) have received enormous attention over the past 5 to 10 years but remain topics of considerable controversy. Opinions about the validity of the CSC hypothesis, the biological properties of CSCs, and the relevance of CSCs to cancer therapy differ widely. In the following commentary, we discuss the nature of the debate, the parameters by which CSCs can or cannot be defined, and the identification of new potential therapeutic targets elucidated by considering cancer as a problem in stem cell biology.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2873047/" 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/PMC2873047/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosen, Jeffrey M -- Jordan, Craig T -- R01 CA122206/CA/NCI NIH HHS/ -- R01 CA122206-02/CA/NCI NIH HHS/ -- R01-CA122206/CA/NCI NIH HHS/ -- R37 CA016303/CA/NCI NIH HHS/ -- R37 CA016303-36/CA/NCI NIH HHS/ -- R37-CA16303/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2009 Jun 26;324(5935):1670-3. doi: 10.1126/science.1171837.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19556499" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Humans ; Mice ; Models, Biological ; Neoplasm Transplantation ; Neoplasms/genetics/metabolism/*pathology/therapy ; Neoplastic Stem Cells/cytology/*physiology ; Transcription, Genetic
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  • 15
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    Circadian control of the NAD+ salvage pathway by CLOCK-SIRT1 (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-17
    Description: Many metabolic and physiological processes display circadian oscillations. We have shown that the core circadian regulator, CLOCK, is a histone acetyltransferase whose activity is counterbalanced by the nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylase SIRT1. Here we show that intracellular NAD+ levels cycle with a 24-hour rhythm, an oscillation driven by the circadian clock. CLOCK:BMAL1 regulates the circadian expression of NAMPT (nicotinamide phosphoribosyltransferase), an enzyme that provides a rate-limiting step in the NAD+ salvage pathway. SIRT1 is recruited to the Nampt promoter and contributes to the circadian synthesis of its own coenzyme. Using the specific inhibitor FK866, we demonstrated that NAMPT is required to modulate circadian gene expression. Our findings in mouse embryo fibroblasts reveal an interlocked transcriptional-enzymatic feedback loop that governs the molecular interplay between cellular metabolism and circadian rhythms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakahata, Yasukazu -- Sahar, Saurabh -- Astarita, Giuseppe -- Kaluzova, Milota -- Sassone-Corsi, Paolo -- R01-GM081634/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2009 May 1;324(5927):654-7. doi: 10.1126/science.1170803. Epub 2009 Mar 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, School of Medicine, University of California, Irvine, Irvine, CA 92697, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19286518" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors ; Acrylamides/pharmacology ; Animals ; Basic Helix-Loop-Helix Transcription Factors/metabolism ; Biological Clocks ; CLOCK Proteins ; Cell Line ; Chromatin Assembly and Disassembly ; *Circadian Rhythm ; Cytokines/antagonists & inhibitors/genetics/*metabolism ; Enzyme Inhibitors/pharmacology ; *Feedback, Physiological ; *Gene Expression Regulation ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Knockout ; NAD/*metabolism ; Niacinamide/metabolism ; Nicotinamide Phosphoribosyltransferase/antagonists & ; inhibitors/genetics/*metabolism ; Piperidines/pharmacology ; Promoter Regions, Genetic ; Sirtuin 1 ; Sirtuins/*metabolism ; Trans-Activators/genetics/*metabolism ; Transcription, Genetic
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  • 16
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    Plant science. Paternal patterning cue (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grossniklaus, Ueli -- New York, N.Y. -- Science. 2009 Mar 13;323(5920):1439-40. doi: 10.1126/science.1171412.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Plant Biology and Zurich-Basel Plant Science Center, University of Zurich, Zollikerstrasse 107, 8008 Zurich, Switzerland. grossnik@botinst.uzh.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19286544" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Arabidopsis/embryology/*genetics/*growth & development/metabolism ; Arabidopsis Proteins/chemistry/*genetics/*metabolism ; Cell Division ; *Gene Expression Regulation, Plant ; Genomic Imprinting ; Interleukin-1 Receptor-Associated Kinases/chemistry/*genetics/*metabolism ; MAP Kinase Kinase Kinases/metabolism ; MAP Kinase Signaling System ; Mitogen-Activated Protein Kinase Kinases/metabolism ; Mitogen-Activated Protein Kinases/metabolism ; Mutation ; Seeds/growth & development/metabolism ; Transcription, Genetic
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  • 17
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    Ribosomal protein S6 kinase 1 signaling regulates mammalian life span (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-10-03
    Description: Caloric restriction (CR) protects against aging and disease, but the mechanisms by which this affects mammalian life span are unclear. We show in mice that deletion of ribosomal S6 protein kinase 1 (S6K1), a component of the nutrient-responsive mTOR (mammalian target of rapamycin) signaling pathway, led to increased life span and resistance to age-related pathologies, such as bone, immune, and motor dysfunction and loss of insulin sensitivity. Deletion of S6K1 induced gene expression patterns similar to those seen in CR or with pharmacological activation of adenosine monophosphate (AMP)-activated protein kinase (AMPK), a conserved regulator of the metabolic response to CR. Our results demonstrate that S6K1 influences healthy mammalian life-span and suggest that therapeutic manipulation of S6K1 and AMPK might mimic CR and could provide broad protection against diseases of aging.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Selman, Colin -- Tullet, Jennifer M A -- Wieser, Daniela -- Irvine, Elaine -- Lingard, Steven J -- Choudhury, Agharul I -- Claret, Marc -- Al-Qassab, Hind -- Carmignac, Danielle -- Ramadani, Faruk -- Woods, Angela -- Robinson, Iain C A -- Schuster, Eugene -- Batterham, Rachel L -- Kozma, Sara C -- Thomas, George -- Carling, David -- Okkenhaug, Klaus -- Thornton, Janet M -- Partridge, Linda -- Gems, David -- Withers, Dominic J -- BBS/E/B/0000C236/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBS/E/B/0000M979/Biotechnology and Biological Sciences Research Council/United Kingdom -- G0800339/Medical Research Council/United Kingdom -- G108/551/Medical Research Council/United Kingdom -- MC_U117531708/Medical Research Council/United Kingdom -- MC_U120027537/Medical Research Council/United Kingdom -- MC_U120097114/Medical Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2009 Oct 2;326(5949):140-4. doi: 10.1126/science.1177221.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Healthy Ageing, Centre for Diabetes and Endocrinology, Department of Medicine, University College London, London WC1E 6JJ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19797661" target="_blank"〉PubMed〈/a〉
    Keywords: AMP-Activated Protein Kinases/metabolism ; Adipose Tissue, White/metabolism ; Aging/*physiology ; Animals ; Bone Density ; Caloric Restriction ; Female ; Gene Deletion ; Gene Expression ; Gene Expression Regulation ; Insulin/metabolism ; Liver/metabolism ; Longevity/*physiology ; Male ; Mice ; Mice, Inbred C57BL ; Motor Activity ; Muscle, Skeletal/metabolism ; Protein Kinases/metabolism ; Ribosomal Protein S6 Kinases, 90-kDa/genetics/*metabolism ; *Signal Transduction ; T-Lymphocyte Subsets/immunology ; TOR Serine-Threonine Kinases ; Transcription, Genetic
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  • 18
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    Targeted 3' processing of antisense transcripts triggers Arabidopsis FLC chromatin silencing (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-08
    Description: Noncoding RNA is emerging as an important regulator of gene expression in many organisms. We are characterizing RNA-mediated chromatin silencing of the Arabidopsis major floral repressor gene, FLC. Through suppressor mutagenesis, we identify a requirement for CstF64 and CstF77, two conserved RNA 3'-end-processing factors, in FLC silencing. However, FLC sense transcript 3' processing is not affected in the mutants. Instead, CstF64 and CstF77 are required for 3' processing of FLC antisense transcripts. A specific RNA-binding protein directs their activity to a proximal antisense polyadenylation site. This targeted processing triggers localized histone demethylase activity and results in reduced FLC sense transcription. Targeted 3' processing of antisense transcripts may be a common mechanism triggering transcriptional silencing of the corresponding sense gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Fuquan -- Marquardt, Sebastian -- Lister, Clare -- Swiezewski, Szymon -- Dean, Caroline -- BB/D010799/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/G01406X/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBS/E/J/000CA305/Biotechnology and Biological Sciences Research Council/United Kingdom -- New York, N.Y. -- Science. 2010 Jan 1;327(5961):94-7. doi: 10.1126/science.1180278. Epub 2009 Dec 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Developmental Biology, John Innes Centre, Norwich NR4 7UH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965720" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/*genetics/growth & development/metabolism ; Arabidopsis Proteins/*genetics/metabolism ; Chromatin/*genetics/metabolism ; Cleavage Stimulation Factor/genetics/metabolism ; Epistasis, Genetic ; Flowers/growth & development ; *Gene Expression Regulation, Plant ; *Gene Silencing ; Histone Deacetylases/genetics/metabolism ; MADS Domain Proteins/*genetics/metabolism ; Models, Genetic ; Polyadenylation ; RNA Processing, Post-Transcriptional ; RNA, Antisense/*metabolism ; RNA, Plant/*metabolism ; RNA-Binding Proteins/genetics/metabolism ; Suppression, Genetic ; Transcription, Genetic ; mRNA Cleavage and Polyadenylation Factors/genetics/metabolism
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  • 19
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    Plant science. DNA binding made easy (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Voytas, Daniel F -- Joung, J Keith -- DP1 OD006862/OD/NIH HHS/ -- New York, N.Y. -- Science. 2009 Dec 11;326(5959):1491-2. doi: 10.1126/science.1183604.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Cell Biology and Development and Center for Genome Engineering, University of Minnesota, Minneapolis, MN 55455, USA. voytas@umn.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20007890" target="_blank"〉PubMed〈/a〉
    Keywords: *Amino Acid Motifs ; Bacterial Proteins/chemistry/metabolism ; Capsicum/genetics/microbiology ; DNA, Plant/chemistry/*metabolism ; DNA-Binding Proteins/chemistry/*metabolism ; Genes, Plant ; Oryza/genetics/microbiology ; Promoter Regions, Genetic ; Repetitive Sequences, Amino Acid ; Transcription, Genetic ; *Transcriptional Activation ; Xanthomonas/*metabolism/pathogenicity
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  • 20
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    ATP-citrate lyase links cellular metabolism to histone acetylation (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-05-23
    Description: Histone acetylation in single-cell eukaryotes relies on acetyl coenzyme A (acetyl-CoA) synthetase enzymes that use acetate to produce acetyl-CoA. Metazoans, however, use glucose as their main carbon source and have exposure only to low concentrations of extracellular acetate. We have shown that histone acetylation in mammalian cells is dependent on adenosine triphosphate (ATP)-citrate lyase (ACL), the enzyme that converts glucose-derived citrate into acetyl-CoA. We found that ACL is required for increases in histone acetylation in response to growth factor stimulation and during differentiation, and that glucose availability can affect histone acetylation in an ACL-dependent manner. Together, these findings suggest that ACL activity is required to link growth factor-induced increases in nutrient metabolism to the regulation of histone acetylation and gene expression.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2746744/" 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/PMC2746744/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wellen, Kathryn E -- Hatzivassiliou, Georgia -- Sachdeva, Uma M -- Bui, Thi V -- Cross, Justin R -- Thompson, Craig B -- R01 CA092660/CA/NCI NIH HHS/ -- R01 CA092660-09/CA/NCI NIH HHS/ -- R01 CA105463/CA/NCI NIH HHS/ -- T32-HL07439-27/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2009 May 22;324(5930):1076-80. doi: 10.1126/science.1164097.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Biology, Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19461003" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; ATP Citrate (pro-S)-Lyase/genetics/*metabolism ; Acetate-CoA Ligase/genetics/metabolism ; Acetyl Coenzyme A/metabolism ; Acetylation ; Adipocytes/cytology/metabolism ; Animals ; Cell Differentiation ; Cell Line ; Cell Line, Tumor ; Cell Nucleus/enzymology ; Cell Proliferation ; Citric Acid/metabolism ; Cytoplasm/enzymology ; Gene Expression Regulation ; Glucose/*metabolism ; Glycolysis ; Histone Deacetylase Inhibitors ; Histone Deacetylases/metabolism ; Histones/*metabolism ; Humans ; Intercellular Signaling Peptides and Proteins/metabolism ; Interleukin-3/metabolism ; Mice ; RNA Interference ; Transcription, Genetic
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  • 21
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    Unbiased reconstruction of a mammalian transcriptional network mediating pathogen responses (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-09-05
    Description: Models of mammalian regulatory networks controlling gene expression have been inferred from genomic data but have largely not been validated. We present an unbiased strategy to systematically perturb candidate regulators and monitor cellular transcriptional responses. We applied this approach to derive regulatory networks that control the transcriptional response of mouse primary dendritic cells to pathogens. Our approach revealed the regulatory functions of 125 transcription factors, chromatin modifiers, and RNA binding proteins, which enabled the construction of a network model consisting of 24 core regulators and 76 fine-tuners that help to explain how pathogen-sensing pathways achieve specificity. This study establishes a broadly applicable, comprehensive, and unbiased approach to reveal the wiring and functions of a regulatory network controlling a major transcriptional response in primary mammalian cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2879337/" 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/PMC2879337/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Amit, Ido -- Garber, Manuel -- Chevrier, Nicolas -- Leite, Ana Paula -- Donner, Yoni -- Eisenhaure, Thomas -- Guttman, Mitchell -- Grenier, Jennifer K -- Li, Weibo -- Zuk, Or -- Schubert, Lisa A -- Birditt, Brian -- Shay, Tal -- Goren, Alon -- Zhang, Xiaolan -- Smith, Zachary -- Deering, Raquel -- McDonald, Rebecca C -- Cabili, Moran -- Bernstein, Bradley E -- Rinn, John L -- Meissner, Alex -- Root, David E -- Hacohen, Nir -- Regev, Aviv -- DP1 OD003958/OD/NIH HHS/ -- DP1 OD003958-01/OD/NIH HHS/ -- DP2 OD002230/OD/NIH HHS/ -- DP2 OD002230-01/OD/NIH HHS/ -- R21 AI071060/AI/NIAID NIH HHS/ -- R21 AI071060-01/AI/NIAID NIH HHS/ -- R21 AI71060/AI/NIAID NIH HHS/ -- S10 RR026688/RR/NCRR NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Oct 9;326(5950):257-63. doi: 10.1126/science.1179050. Epub 2009 Sep 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Broad Institute of MIT and Harvard, 7 Cambridge Center, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19729616" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacteria/*immunology ; Chromatin Assembly and Disassembly ; DNA, Single-Stranded/immunology ; Dendritic Cells/*immunology/*metabolism ; Feedback, Physiological ; Gene Expression Profiling ; *Gene Expression Regulation ; *Gene Regulatory Networks ; Inflammation/immunology/*metabolism ; Lipopeptides/immunology ; Lipopolysaccharides/immunology ; Mice ; Mice, Inbred C57BL ; Poly I-C/immunology ; RNA-Binding Proteins/metabolism ; Toll-Like Receptors/agonists ; Transcription Factors/metabolism ; Transcription, Genetic ; Viruses/*immunology
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    RNA Pol II accumulates at promoters of growth genes during developmental arrest (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-03
    Description: When Caenorhabditis elegans larvae hatch from the egg case in the absence of food, their development is arrested (L1 arrest), and they show increased stress resistance until food becomes available. To study nutritional control of larval development, we analyzed growth and gene expression profiles during L1 arrest and recovery. Larvae that were fed responded relatively slowly to starvation compared with the rapid response of arrested larvae to feeding. Chromatin immunoprecipitation of RNA polymerase II (Pol II) followed by deep sequencing showed that during L1 arrest, Pol II continued transcribing starvation-response genes, but the enzyme accumulated on the promoters of growth and development genes. In response to feeding, promoter accumulation decreased, and elongation and messenger RNA levels increased. Therefore, accumulation of Pol II at promoters anticipates nutritionally controlled gene expression during C. elegans development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baugh, L Ryan -- Demodena, John -- Sternberg, Paul W -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Apr 3;324(5923):92-4. doi: 10.1126/science.1169628. Epub 2009 Feb 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19251593" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/*genetics/*growth & development/metabolism ; Chromatin Immunoprecipitation ; Cluster Analysis ; Escherichia coli ; Food ; Gene Expression Profiling ; *Gene Expression Regulation, Developmental ; Genes, Helminth ; Nutritional Physiological Phenomena ; Oligonucleotide Array Sequence Analysis ; Principal Component Analysis ; *Promoter Regions, Genetic ; RNA Polymerase II/*metabolism ; RNA, Helminth/genetics/metabolism ; RNA, Messenger/genetics/metabolism ; Signal Transduction ; Starvation ; Transcription, Genetic ; Up-Regulation
    Print ISSN: 0036-8075
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  • 23
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    Circadian clock feedback cycle through NAMPT-mediated NAD+ biosynthesis (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-21
    Description: The circadian clock is encoded by a transcription-translation feedback loop that synchronizes behavior and metabolism with the light-dark cycle. Here we report that both the rate-limiting enzyme in mammalian nicotinamide adenine dinucleotide (NAD+) biosynthesis, nicotinamide phosphoribosyltransferase (NAMPT), and levels of NAD+ display circadian oscillations that are regulated by the core clock machinery in mice. Inhibition of NAMPT promotes oscillation of the clock gene Per2 by releasing CLOCK:BMAL1 from suppression by SIRT1. In turn, the circadian transcription factor CLOCK binds to and up-regulates Nampt, thus completing a feedback loop involving NAMPT/NAD+ and SIRT1/CLOCK:BMAL1.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2738420/" 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/PMC2738420/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ramsey, Kathryn Moynihan -- Yoshino, Jun -- Brace, Cynthia S -- Abrassart, Dana -- Kobayashi, Yumiko -- Marcheva, Biliana -- Hong, Hee-Kyung -- Chong, Jason L -- Buhr, Ethan D -- Lee, Choogon -- Takahashi, Joseph S -- Imai, Shin-Ichiro -- Bass, Joseph -- AG02150/AG/NIA NIH HHS/ -- P01 AG011412/AG/NIA NIH HHS/ -- P50 MH074924/MH/NIMH NIH HHS/ -- R01 AG024150/AG/NIA NIH HHS/ -- R01 AG024150-05/AG/NIA NIH HHS/ -- T32 DK007169/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 May 1;324(5927):651-4. doi: 10.1126/science.1171641. Epub 2009 Mar 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Northwestern University Feinberg School of Medicine, 2200 Campus Drive, Evanston, IL 60208-3500, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19299583" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors ; Acrylamides/pharmacology ; Adipose Tissue, White/metabolism ; Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics/metabolism ; *Biological Clocks ; CLOCK Proteins ; Cell Cycle Proteins/genetics ; Cell Line ; Cell Line, Tumor ; *Circadian Rhythm ; Cytokines/antagonists & inhibitors/genetics/*metabolism ; Enzyme Inhibitors/pharmacology ; *Feedback, Physiological ; Gene Expression Regulation ; Hepatocytes/metabolism ; Humans ; Liver/metabolism ; Mice ; NAD/*biosynthesis ; Nicotinamide Phosphoribosyltransferase/antagonists & ; inhibitors/genetics/*metabolism ; Nuclear Proteins/genetics ; Period Circadian Proteins ; Piperidines/pharmacology ; Protein Binding ; Sirtuin 1 ; Sirtuins/metabolism ; Trans-Activators/genetics/metabolism ; Transcription Factors/genetics ; Transcription, Genetic
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    Epigenetic temporal control of mouse Hox genes in vivo (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-06-06
    Description: During vertebrate development, the temporal control of Hox gene transcriptional activation follows the genomic order of the genes within the Hox clusters. Although it is recognized that this "Hox clock" serves to coordinate body patterning, the underlying mechanism remains elusive. We have shown that successive Hox gene activation in the mouse embryo is closely associated with a directional transition in chromatin status, as judged by the dynamic progression of transcription-competent modifications: Increases in activation marks correspond to decreases in repressive marks. Furthermore, using a mouse in which a Hox cluster was split into two pieces, we document the necessity to maintain a clustered organization to properly implement this process. These results suggest that chromatin modifications are important parameters in the temporal regulation of this gene family.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Soshnikova, Natalia -- Duboule, Denis -- New York, N.Y. -- Science. 2009 Jun 5;324(5932):1320-3. doi: 10.1126/science.1171468.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Research Centre Frontiers in Genetics, Department of Zoology and Animal Biology, University of Geneva, Sciences III, Quai Ernest-Ansermet 30, 1211 Geneva 4, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19498168" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Body Patterning ; Chromatin/*metabolism ; Embryo, Mammalian/*physiology ; *Embryonic Development ; *Epigenesis, Genetic ; Gene Expression Profiling ; *Gene Expression Regulation, Developmental ; *Genes, Homeobox ; Histones/metabolism ; Methylation ; Mice ; Multigene Family ; RNA Polymerase II/metabolism ; Transcription, Genetic ; *Transcriptional Activation
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    Essential role of the glycosyltransferase sxc/Ogt in polycomb repression (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-30
    Description: Polycomb group proteins are conserved transcriptional repressors that control animal and plant development. Here, we found that the Drosophila Polycomb group gene super sex combs (sxc) encodes Ogt, the highly conserved glycosyltransferase that catalyzes the addition of N-acetylglucosamine (GlcNAc) to proteins in animals and plants. Genome-wide profiling in Drosophila revealed that GlcNAc-modified proteins are highly enriched at Polycomb response elements. Among different Polycomb group proteins, Polyhomeotic is glycosylated by Sxc/Ogt in vivo. sxc/Ogt-null mutants lacked O-linked GlcNAcylation and failed to maintain Polycomb transcriptional repression even though Polycomb group protein complexes were bound at their target sites. Polycomb repression appears to be a critical function of Sxc/Ogt in Drosophila and may be mediated by the glycosylation of Polyhomeotic.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gambetta, Maria Cristina -- Oktaba, Katarzyna -- Muller, Jurg -- New York, N.Y. -- Science. 2009 Jul 3;325(5936):93-6. doi: 10.1126/science.1169727. Epub 2009 May 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gene Expression Programme, European Molecular Biology Laboratory (EMBL), Meyerhofstrasse 1, 69117 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19478141" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylglucosamine/*metabolism ; Animals ; Chromatin/metabolism ; Chromatin Immunoprecipitation ; DNA-Binding Proteins/*metabolism ; Drosophila Proteins/*genetics/*metabolism ; Drosophila melanogaster/*genetics/*metabolism ; *Gene Silencing ; Genes, Insect ; Glycosylation ; Nucleoproteins/*metabolism ; Polycomb Repressive Complex 1 ; Polycomb-Group Proteins ; Protein Binding ; Protein Subunits/metabolism ; Repressor Proteins/chemistry/genetics/*metabolism ; Transcription, Genetic
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    LXR regulates cholesterol uptake through Idol-dependent ubiquitination of the LDL receptor (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-06-13
    Description: Cellular cholesterol levels reflect a balance between uptake, efflux, and endogenous synthesis. Here we show that the sterol-responsive nuclear liver X receptor (LXR) helps maintain cholesterol homeostasis, not only through promotion of cholesterol efflux but also through suppression of low-density lipoprotein (LDL) uptake. LXR inhibits the LDL receptor (LDLR) pathway through transcriptional induction of Idol (inducible degrader of the LDLR), an E3 ubiquitin ligase that triggers ubiquitination of the LDLR on its cytoplasmic domain, thereby targeting it for degradation. LXR ligand reduces, whereas LXR knockout increases, LDLR protein levels in vivo in a tissue-selective manner. Idol knockdown in hepatocytes increases LDLR protein levels and promotes LDL uptake. Conversely, adenovirus-mediated expression of Idol in mouse liver promotes LDLR degradation and elevates plasma LDL levels. The LXR-Idol-LDLR axis defines a complementary pathway to sterol response element-binding proteins for sterol regulation of cholesterol uptake.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2777523/" 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/PMC2777523/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zelcer, Noam -- Hong, Cynthia -- Boyadjian, Rima -- Tontonoz, Peter -- HL030568/HL/NHLBI NIH HHS/ -- HL066088/HL/NHLBI NIH HHS/ -- HL090553/HL/NHLBI NIH HHS/ -- P01 HL090553/HL/NHLBI NIH HHS/ -- P01 HL090553-01A10003/HL/NHLBI NIH HHS/ -- R01 HL066088/HL/NHLBI NIH HHS/ -- R01 HL066088-09/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Jul 3;325(5936):100-4. doi: 10.1126/science.1168974. Epub 2009 Jun 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Pathology and Laboratory Medicine, University of California, Los Angeles (UCLA), Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19520913" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line, Tumor ; Cholesterol/*metabolism ; DNA-Binding Proteins/agonists/*metabolism ; Homeostasis ; Humans ; Ligands ; Lipoproteins, LDL/blood/metabolism ; Liver/metabolism ; Mice ; Mice, Inbred C57BL ; Orphan Nuclear Receptors ; Promoter Regions, Genetic ; RNA, Messenger/genetics/metabolism ; Receptors, Cytoplasmic and Nuclear/agonists/*metabolism ; Receptors, LDL/genetics/*metabolism ; Transcription, Genetic ; Ubiquitin-Protein Ligases ; Ubiquitination
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    Neuroscience. Nuclear power for axonal growth (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-10-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Subang, M C -- Richardson, P M -- New York, N.Y. -- Science. 2009 Oct 9;326(5950):238-9. doi: 10.1126/science.1181038.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Bone and Joint Research, Barts and the London School of Medicine, Charterhouse Square, London EC1M 6BQ, UK. m.c.subang@qmul.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19815761" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology/ultrastructure ; Cell Nucleus/*metabolism ; Cytoskeleton/metabolism ; Growth Cones/*physiology/ultrastructure ; Hippocampus/cytology/embryology ; Intercellular Signaling Peptides and Proteins/metabolism ; Kruppel-Like Transcription Factors/genetics/*metabolism ; Mice ; Nerve Regeneration ; Nerve Tissue Proteins/metabolism ; Rats ; Retinal Ganglion Cells/cytology ; Transcription Factors/metabolism ; Transcription, Genetic
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  • 28
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    A functional genomics approach reveals CHE as a component of the Arabidopsis circadian clock (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-17
    Description: Transcriptional feedback loops constitute the molecular circuitry of the plant circadian clock. In Arabidopsis, a core loop is established between CCA1 and TOC1. Although CCA1 directly represses TOC1, the TOC1 protein has no DNA binding domains, which suggests that it cannot directly regulate CCA1. We established a functional genomic strategy that led to the identification of CHE, a TCP transcription factor that binds specifically to the CCA1 promoter. CHE is a clock component partially redundant with LHY in the repression of CCA1. The expression of CHE is regulated by CCA1, thus adding a CCA1/CHE feedback loop to the Arabidopsis circadian network. Because CHE and TOC1 interact, and CHE binds to the CCA1 promoter, a molecular linkage between TOC1 and CCA1 gene regulation is established.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4259050/" 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/PMC4259050/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pruneda-Paz, Jose L -- Breton, Ghislain -- Para, Alessia -- Kay, Steve A -- GM56006/GM/NIGMS NIH HHS/ -- GM67837/GM/NIGMS NIH HHS/ -- R01 GM056006/GM/NIGMS NIH HHS/ -- R01 GM067837/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2009 Mar 13;323(5920):1481-5. doi: 10.1126/science.1167206.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Cell and Developmental Biology, Division of Biological Sciences, University of California San Diego, La Jolla, CA 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19286557" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Arabidopsis/genetics/metabolism/*physiology ; Arabidopsis Proteins/chemistry/*genetics/*metabolism ; Binding Sites ; Biological Clocks/*genetics ; Cell Nucleus/metabolism ; Circadian Rhythm/*genetics ; DNA-Binding Proteins/genetics/metabolism ; Feedback, Physiological ; *Gene Expression Regulation, Plant ; Genes, Plant ; Genomics ; Molecular Sequence Data ; Plants, Genetically Modified ; Promoter Regions, Genetic ; Repressor Proteins/chemistry/*genetics/*metabolism ; Transcription Factors/*genetics/metabolism ; Transcription, Genetic
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    Systems biology. Excavating the functional landscape of bacterial cells (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ochman, Howard -- Raghavan, Rahul -- New York, N.Y. -- Science. 2009 Nov 27;326(5957):1200-1. doi: 10.1126/science.1183757.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ecology and Evolutionary Biology, University of Arizona, Tucson, AZ 85718, USA. hochman@email.arizona.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965458" target="_blank"〉PubMed〈/a〉
    Keywords: Bacterial Proteins/*metabolism ; Culture Media ; Gene Expression Profiling ; *Gene Expression Regulation, Bacterial ; *Genome, Bacterial ; *Metabolic Networks and Pathways ; Mycoplasma pneumoniae/*genetics/growth & development/*metabolism ; Protein Interaction Mapping ; Regulatory Elements, Transcriptional ; Systems Biology ; Transcription, Genetic
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  • 30
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    Cell signaling in space and time: where proteins come together and when they're apart (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-12-08
    Description: Signal transduction can be defined as the coordinated relay of messages derived from extracellular cues to intracellular effectors. More simply put, information received on the cell surface is processed across the plasma membrane and transmitted to intracellular targets. This requires that the activators, effectors, enzymes, and substrates that respond to cellular signals come together when they need to.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3041271/" 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/PMC3041271/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scott, John D -- Pawson, Tony -- 57793/Canadian Institutes of Health Research/Canada -- 6849/Canadian Institutes of Health Research/Canada -- GM48231/GM/NIGMS NIH HHS/ -- R37 GM048231/GM/NIGMS NIH HHS/ -- R37 GM048231-19/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Nov 27;326(5957):1220-4. doi: 10.1126/science.1175668.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Howard Hughes Medical Institute, Box 357750, University of Washington School of Medicine, Seattle, WA 98195, USA. scottjdw@u.washington.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965465" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Compartmentation ; Cell Membrane/*metabolism ; Cell Nucleus/*metabolism ; Cytoplasm/*metabolism ; Enzymes/metabolism ; Humans ; MAP Kinase Signaling System ; Models, Biological ; Multiprotein Complexes/metabolism ; Protein Interaction Domains and Motifs ; Proteins/*metabolism ; *Signal Transduction ; Time Factors ; Transcription, Genetic
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    Suppression of the microRNA pathway by bacterial effector proteins (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-08-16
    Description: Plants and animals sense pathogen-associated molecular patterns (PAMPs) and in turn differentially regulate a subset of microRNAs (miRNAs). However, the extent to which the miRNA pathway contributes to innate immunity remains unknown. Here, we show that miRNA-deficient mutants of Arabidopsis partly restore growth of a type III secretion-defective mutant of Pseudomonas syringae. These mutants also sustained growth of nonpathogenic Pseudomonas fluorescens and Escherichia coli strains, implicating miRNAs as key components of plant basal defense. Accordingly, we have identified P. syringae effectors that suppress transcriptional activation of some PAMP-responsive miRNAs or miRNA biogenesis, stability, or activity. These results provide evidence that, like viruses, bacteria have evolved to suppress RNA silencing to cause disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2570098/" 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/PMC2570098/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Navarro, Lionel -- Jay, Florence -- Nomura, Kinya -- He, Sheng Yang -- Voinnet, Olivier -- 5R01AI060761/AI/NIAID NIH HHS/ -- R01 AI060761/AI/NIAID NIH HHS/ -- R01 AI060761-03/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2008 Aug 15;321(5891):964-7. doi: 10.1126/science.1159505.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Biologie Moleculaire des Plantes, CNRS UPR 2353-Universite Louis Pasteur, 12 Rue du General Zimmer, 67084 Strasbourg Cedex, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18703740" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/genetics/immunology/*microbiology/virology ; Bacterial Proteins/*metabolism ; Escherichia coli/growth & development ; Immunity, Innate ; MicroRNAs/genetics/*metabolism ; Mutation ; Plant Diseases/immunology/*microbiology ; Plant Leaves/metabolism/microbiology ; Plants, Genetically Modified ; Potyvirus/physiology ; Pseudomonas fluorescens/growth & development ; Pseudomonas syringae/genetics/*growth & development/metabolism/pathogenicity ; RNA Interference ; RNA Stability ; RNA, Plant/genetics/*metabolism ; Transcription, Genetic
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    Regulation of CD45 alternative splicing by heterogeneous ribonucleoprotein, hnRNPLL (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-08-02
    Description: The transition from naive to activated T cells is marked by alternative splicing of pre-mRNA encoding the transmembrane phosphatase CD45. Using a short hairpin RNA interference screen, we identified heterogeneous ribonucleoprotein L-like (hnRNPLL) as a critical inducible regulator of CD45 alternative splicing. HnRNPLL was up-regulated in stimulated T cells, bound CD45 transcripts, and was both necessary and sufficient for CD45 alternative splicing. Depletion or overexpression of hnRNPLL in B and T cell lines and primary T cells resulted in reciprocal alteration of CD45RA and RO expression. Exon array analysis suggested that hnRNPLL acts as a global regulator of alternative splicing in activated T cells. Induction of hnRNPLL during hematopoietic cell activation and differentiation may allow cells to rapidly shift their transcriptomes to favor proliferation and inhibit cell death.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2791692/" 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/PMC2791692/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oberdoerffer, Shalini -- Moita, Luis Ferreira -- Neems, Daniel -- Freitas, Rui P -- Hacohen, Nir -- Rao, Anjana -- AI40127/AI/NIAID NIH HHS/ -- AI44432/AI/NIAID NIH HHS/ -- CA42471/CA/NCI NIH HHS/ -- R01 AI040127/AI/NIAID NIH HHS/ -- R01 AI040127-18/AI/NIAID NIH HHS/ -- R01 AI040127-19/AI/NIAID NIH HHS/ -- R01 AI044432/AI/NIAID NIH HHS/ -- R01 AI044432-09/AI/NIAID NIH HHS/ -- R01 AI044432-10/AI/NIAID NIH HHS/ -- R01 AI080875/AI/NIAID NIH HHS/ -- R01 AI080875-01/AI/NIAID NIH HHS/ -- R01 CA042471/CA/NCI NIH HHS/ -- R01 CA042471-23/CA/NCI NIH HHS/ -- R21 AI071060/AI/NIAID NIH HHS/ -- R21 AI071060-01/AI/NIAID NIH HHS/ -- R21 AI071060-02/AI/NIAID NIH HHS/ -- T32 HL066987/HL/NHLBI NIH HHS/ -- U19 AI070352/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2008 Aug 1;321(5889):686-91. doi: 10.1126/science.1157610. Epub 2008 Jul 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Immune Disease Institute, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18669861" target="_blank"〉PubMed〈/a〉
    Keywords: *Alternative Splicing ; Antigens, CD45/chemistry/*genetics ; B-Lymphocytes/immunology/metabolism ; CD4-Positive T-Lymphocytes/*immunology/*metabolism ; Cell Line ; Cell Line, Tumor ; Heterogeneous-Nuclear Ribonucleoproteins/genetics/*metabolism ; Humans ; Lentivirus/genetics/physiology ; *Lymphocyte Activation ; Protein Isoforms/chemistry/genetics ; RNA Interference ; STAT5 Transcription Factor/genetics ; T-Lymphocytes/*immunology/*metabolism ; Tetradecanoylphorbol Acetate/pharmacology ; Transcription, Genetic ; Transduction, Genetic ; Up-Regulation
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    Tight regulation of unstructured proteins: from transcript synthesis to protein degradation (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-11-29
    Description: Altered abundance of several intrinsically unstructured proteins (IUPs) has been associated with perturbed cellular signaling that may lead to pathological conditions such as cancer. Therefore, it is important to understand how cells precisely regulate the availability of IUPs. We observed that regulation of transcript clearance, proteolytic degradation, and translational rate contribute to controlling the abundance of IUPs, some of which are present in low amounts and for short periods of time. Abundant phosphorylation and low stochasticity in transcription and translation indicate that the availability of IUPs can be finely tuned. Fidelity in signaling may require that most IUPs be available in appropriate amounts and not present longer than needed.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2803065/" 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/PMC2803065/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gsponer, Jorg -- Futschik, Matthias E -- Teichmann, Sarah A -- Babu, M Madan -- G0600158/Medical Research Council/United Kingdom -- MC_U105161047/Medical Research Council/United Kingdom -- MC_U105185859/Medical Research Council/United Kingdom -- U.1051.04.027.00001.01 (85859)/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2008 Nov 28;322(5906):1365-8. doi: 10.1126/science.1163581.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council (MRC) Laboratory of Molecular Biology, Hills Road, Cambridge CB2 0QH, UK. jgsponer@mrc-lmb.cam.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19039133" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Cell Cycle ; Computational Biology ; Genes, Fungal ; Humans ; Phosphorylation ; Protein Biosynthesis ; Protein Conformation ; Protein Kinases/metabolism ; Proteome/chemistry ; RNA, Fungal/genetics/metabolism ; RNA, Messenger/genetics/metabolism ; Saccharomyces cerevisiae/chemistry/cytology/genetics/*metabolism ; Saccharomyces cerevisiae Proteins/*chemistry/genetics/*metabolism ; Schizosaccharomyces pombe Proteins/chemistry/metabolism ; Signal Transduction ; Transcription, Genetic
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    cAMP-dependent signaling as a core component of the mammalian circadian pacemaker (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-05-20
    Description: The mammalian circadian clockwork is modeled as transcriptional and posttranslational feedback loops, whereby circadian genes are periodically suppressed by their protein products. We show that adenosine 3',5'-monophosphate (cAMP) signaling constitutes an additional, bona fide component of the oscillatory network. cAMP signaling is rhythmic and sustains the transcriptional loop of the suprachiasmatic nucleus, determining canonical pacemaker properties of amplitude, phase, and period. This role is general and is evident in peripheral mammalian tissues and cell lines, which reveals an unanticipated point of circadian regulation in mammals qualitatively different from the existing transcriptional feedback model. We propose that daily activation of cAMP signaling, driven by the transcriptional oscillator, in turn sustains progression of transcriptional rhythms. In this way, clock output constitutes an input to subsequent cycles.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2735813/" 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/PMC2735813/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Neill, John S -- Maywood, Elizabeth S -- Chesham, Johanna E -- Takahashi, Joseph S -- Hastings, Michael H -- MC_U105170643/Medical Research Council/United Kingdom -- U.1051.02.004(78799)/Medical Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Howard Hughes Medical Institute/ -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2008 May 16;320(5878):949-53. doi: 10.1126/science.1152506.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council (MRC) Laboratory of Molecular Biology, Hills Road, Cambridge CB2 0QH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18487196" target="_blank"〉PubMed〈/a〉
    Keywords: Adenine/analogs & derivatives/pharmacology ; Adenylyl Cyclase Inhibitors ; Adenylyl Cyclases/metabolism ; Animals ; Biological Clocks/genetics/*physiology ; Cell Cycle Proteins/genetics/metabolism ; Circadian Rhythm/drug effects/genetics/*physiology ; Cyclic AMP/*metabolism ; Enzyme Inhibitors/pharmacology ; Feedback, Physiological ; Gene Expression Regulation/drug effects ; Guanine Nucleotide Exchange Factors/metabolism ; Mice ; Mice, Transgenic ; NIH 3T3 Cells ; Nuclear Proteins/genetics/metabolism ; Period Circadian Proteins ; Response Elements ; *Signal Transduction ; Suprachiasmatic Nucleus/drug effects/*metabolism ; Transcription Factors/genetics/metabolism ; Transcription, Genetic
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  • 35
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    Termination factor Rho and its cofactors NusA and NusG silence foreign DNA in E. coli (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-05-20
    Description: Transcription of the bacterial genome by the RNA polymerase must terminate at specific points. Transcription can be terminated by Rho factor, an essential protein in enterobacteria. We used the antibiotic bicyclomycin, which inhibits Rho, to assess its role on a genome-wide scale. Rho is revealed as a global regulator of gene expression that matches Escherichia coli transcription to translational needs. We also found that genes in E. coli that are most repressed by Rho are prophages and other horizontally acquired portions of the genome. Elimination of these foreign DNA elements increases resistance to bicyclomycin. Although rho remains essential, such reduced-genome bacteria no longer require Rho cofactors NusA and NusG. Deletion of the cryptic rac prophage in wild-type E. coli increases bicyclomycin resistance and permits deletion of nusG. Thus, Rho termination, supported by NusA and NusG, is required to suppress the toxic activity of foreign genes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4059013/" 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/PMC4059013/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cardinale, Christopher J -- Washburn, Robert S -- Tadigotla, Vasisht R -- Brown, Lewis M -- Gottesman, Max E -- Nudler, Evgeny -- GM72814/GM/NIGMS NIH HHS/ -- R01 GM058750/GM/NIGMS NIH HHS/ -- R01 GM072814/GM/NIGMS NIH HHS/ -- R01 GM37219/GM/NIGMS NIH HHS/ -- R01 GM58750/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2008 May 16;320(5878):935-8. doi: 10.1126/science.1152763.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, New York University School of Medicine, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18487194" target="_blank"〉PubMed〈/a〉
    Keywords: Anti-Bacterial Agents/pharmacology ; Bacteriophage lambda/genetics ; Bicyclo Compounds, Heterocyclic/pharmacology ; Coliphages/genetics ; DNA, Intergenic ; Escherichia coli/drug effects/*genetics/metabolism ; Escherichia coli O157/*genetics/metabolism ; Escherichia coli Proteins/genetics/*metabolism ; Gene Expression Regulation, Bacterial ; *Gene Silencing ; Genome, Bacterial ; Oligonucleotide Array Sequence Analysis ; Peptide Elongation Factors/*metabolism ; Prophages/*genetics ; Proteome ; Rho Factor/antagonists & inhibitors/*metabolism ; Transcription Factors/*metabolism ; Transcription, Genetic ; Transcriptional Elongation Factors
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    Physiology. Unfolding lipid metabolism (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-06-17
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2701207/" 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/PMC2701207/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Horton, Jay D -- P01 HL020948/HL/NHLBI NIH HHS/ -- P01 HL020948-280017/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2008 Jun 13;320(5882):1433-4. doi: 10.1126/science.1159651.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard, Dallas, TX 75390-9046, USA. jay.horton@utsouthwestern.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18556540" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cholesterol/*biosynthesis/blood ; DNA-Binding Proteins/genetics/*metabolism ; Endoplasmic Reticulum/metabolism ; Fatty Acids/*biosynthesis ; Gene Deletion ; Gene Expression Regulation ; Lipids/biosynthesis ; *Lipogenesis ; Liver/*metabolism ; Mice ; Nuclear Proteins/genetics/*metabolism ; Protein Folding ; Sterol Regulatory Element Binding Proteins/genetics/metabolism ; Transcription Factors/genetics/*physiology ; Transcription, Genetic ; Triglycerides/blood
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    Absence of the SRC-2 coactivator results in a glycogenopathy resembling Von Gierke's disease (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-11-29
    Description: Hepatic glucose production is critical for basal brain function and survival when dietary glucose is unavailable. Glucose-6-phosphatase (G6Pase) is an essential, rate-limiting enzyme that serves as a terminal gatekeeper for hepatic glucose release into the plasma. Mutations in G6Pase result in Von Gierke's disease (glycogen storage disease-1a), a potentially fatal genetic disorder. We have identified the transcriptional coactivator SRC-2 as a regulator of fasting hepatic glucose release, a function that SRC-2 performs by controlling the expression of hepatic G6Pase. SRC-2 modulates G6Pase expression directly by acting as a coactivator with the orphan nuclear receptor RORalpha. In addition, SRC-2 ablation, in both a whole-body and liver-specific manner, resulted in a Von Gierke's disease phenotype in mice. Our results position SRC-2 as a critical regulator of mammalian glucose production.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2668604/" 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/PMC2668604/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chopra, Atul R -- Louet, Jean-Francois -- Saha, Pradip -- An, Jie -- Demayo, Franco -- Xu, Jianming -- York, Brian -- Karpen, Saul -- Finegold, Milton -- Moore, David -- Chan, Lawrence -- Newgard, Christopher B -- O'Malley, Bert W -- DK58242/DK/NIDDK NIH HHS/ -- HL51586/HL/NHLBI NIH HHS/ -- P01 DK059820/DK/NIDDK NIH HHS/ -- P01 DK059820-08/DK/NIDDK NIH HHS/ -- P01 DK58398/DK/NIDDK NIH HHS/ -- P01 DK59820/DK/NIDDK NIH HHS/ -- R01 DK056239/DK/NIDDK NIH HHS/ -- R01 DK056239-08/DK/NIDDK NIH HHS/ -- U19 DK062434/DK/NIDDK NIH HHS/ -- U19 DK062434-07/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2008 Nov 28;322(5906):1395-9. doi: 10.1126/science.1164847.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Baylor College of Medicine, 1 Baylor Plaza, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19039140" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Fasting ; Female ; Gene Expression Profiling ; Gene Expression Regulation, Enzymologic ; Glucose/*metabolism ; Glucose-6-Phosphatase/*genetics/metabolism ; Glycogen Storage Disease Type I/*genetics/metabolism ; Hepatocytes/metabolism ; Kidney/metabolism ; Liver/*metabolism ; Liver Glycogen/metabolism ; Male ; Mice ; Mice, Knockout ; Nuclear Receptor Coactivator 2/genetics/*metabolism ; RNA Interference ; Receptors, Retinoic Acid/metabolism ; Response Elements ; Transcription, Genetic ; Triglycerides/metabolism
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    A retrotransposon-mediated gene duplication underlies morphological variation of tomato fruit (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-03-15
    Description: Edible fruits, such as that of the tomato plant and other vegetable crops, are markedly diverse in shape and size. SUN, one of the major genes controlling the elongated fruit shape of tomato, was positionally cloned and found to encode a member of the IQ67 domain-containing family. We show that the locus arose as a result of an unusual 24.7-kilobase gene duplication event mediated by the long terminal repeat retrotransposon Rider. This event resulted in a new genomic context that increased SUN expression relative to that of the ancestral copy, culminating in an elongated fruit shape. Our discovery demonstrates that retrotransposons may be a major driving force in genome evolution and gene duplication, resulting in phenotypic change in plants.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xiao, Han -- Jiang, Ning -- Schaffner, Erin -- Stockinger, Eric J -- van der Knaap, Esther -- New York, N.Y. -- Science. 2008 Mar 14;319(5869):1527-30. doi: 10.1126/science.1153040.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Horticulture and Crop Science, Ohio State University/Ohio Agricultural Research and Development Center, Wooster, OH 44691, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18339939" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Evolution, Molecular ; Fruit/*anatomy & histology ; *Gene Duplication ; Gene Expression Regulation, Plant ; *Genes, Plant ; Genome, Plant ; Lycopersicon esculentum/*anatomy & histology/*genetics ; Molecular Sequence Data ; Phenotype ; Plant Proteins/chemistry/genetics/metabolism ; *Retroelements ; Terminal Repeat Sequences ; Transcription, Genetic ; Transformation, Genetic
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    Gene regulation by transcription factors and microRNAs (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-03-29
    Description: The properties of a cell are determined by the genetic information encoded in its genome. Understanding how such information is differentially and dynamically retrieved to define distinct cell types and cellular states is a major challenge facing molecular biology. Gene regulatory factors that control the expression of genomic information come in a variety of flavors, with transcription factors and microRNAs representing the most numerous gene regulatory factors in multicellular genomes. Here, I review common principles of transcription factor- and microRNA-mediated gene regulatory events and discuss conceptual differences in how these factors control gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hobert, Oliver -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Mar 28;319(5871):1785-6. doi: 10.1126/science.1151651.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Biochemistry and Molecular Biophysics, Columbia University Medical Center, New York, NY 10032, USA. or38@columbia.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18369135" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Gene Expression Regulation ; *Gene Regulatory Networks ; MicroRNAs/genetics/*metabolism ; Phenotype ; Transcription Factors/*metabolism ; Transcription, Genetic
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    Epigenetic reprogramming by adenovirus e1a (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-08-23
    Description: Adenovirus e1a induces quiescent human cells to replicate. We found that e1a causes global relocalization of the RB (retinoblastoma) proteins (RB, p130, and p107) and p300/CBP histone acetyltransferases on promoters, the effect of which is to restrict the acetylation of histone 3 lysine-18 (H3K18ac) to a limited set of genes, thereby stimulating cell cycling and inhibiting antiviral responses and cellular differentiation. Soon after expression, e1a binds transiently to promoters of cell cycle and growth genes, causing enrichment of p300/CBP, PCAF (p300/CBP-associated factor), and H3K18ac; depletion of RB proteins; and transcriptional activation. e1a also associates transiently with promoters of antiviral genes, causing enrichment for RB, p130, and H4K16ac; increased nucleosome density; and transcriptional repression. At later times, e1a and p107 bind mainly to promoters of development and differentiation genes, repressing transcription. The temporal order of e1a binding requires its interactions with p300/CBP and RB proteins. Our data uncover a defined epigenetic reprogramming leading to cellular transformation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2693122/" 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/PMC2693122/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ferrari, Roberto -- Pellegrini, Matteo -- Horwitz, Gregory A -- Xie, Wei -- Berk, Arnold J -- Kurdistani, Siavash K -- CA25235/CA/NCI NIH HHS/ -- R37 CA025235/CA/NCI NIH HHS/ -- R37 CA025235-30/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Aug 22;321(5892):1086-8. doi: 10.1126/science.1155546.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry, University of California, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18719284" target="_blank"〉PubMed〈/a〉
    Keywords: Adenovirus E1A Proteins/genetics/*metabolism ; Adenoviruses, Human/genetics/*metabolism ; CREB-Binding Protein/metabolism ; Cell Transformation, Viral ; Crk-Associated Substrate Protein/genetics/metabolism ; *Epigenesis, Genetic ; Gene Expression Profiling ; Gene Expression Regulation ; Histones/metabolism ; Humans ; Mutation ; Promoter Regions, Genetic ; Protein Binding ; RNA, Messenger/genetics/metabolism ; Retinoblastoma Protein/genetics/metabolism ; Retinoblastoma-Like Protein p107/genetics/metabolism ; Transcription, Genetic ; p300-CBP Transcription Factors/metabolism
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    NADP regulates the yeast GAL induction system (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-02-23
    Description: Transcriptional regulation of the galactose-metabolizing genes in Saccharomyces cerevisiae depends on three core proteins: Gal4p, the transcriptional activator that binds to upstream activating DNA sequences (UAS(GAL)); Gal80p, a repressor that binds to the carboxyl terminus of Gal4p and inhibits transcription; and Gal3p, a cytoplasmic transducer that, upon binding galactose and adenosine 5'-triphosphate, relieves Gal80p repression. The current model of induction relies on Gal3p sequestering Gal80p in the cytoplasm. However, the rapid induction of this system implies that there is a missing factor. Our structure of Gal80p in complex with a peptide from the carboxyl-terminal activation domain of Gal4p reveals the existence of a dinucleotide that mediates the interaction between the two. Biochemical and in vivo experiments suggests that nicotinamide adenine dinucleotide phosphate (NADP) plays a key role in the initial induction event.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2726985/" 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/PMC2726985/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kumar, P Rajesh -- Yu, Yao -- Sternglanz, Rolf -- Johnston, Stephen Albert -- Joshua-Tor, Leemor -- GM074075/GM/NIGMS NIH HHS/ -- GM55641/GM/NIGMS NIH HHS/ -- P30 CA045508/CA/NCI NIH HHS/ -- R01 GM074075/GM/NIGMS NIH HHS/ -- R01 GM074075-04/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Feb 22;319(5866):1090-2. doi: 10.1126/science.1151903.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring Harbor, NY11724, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18292341" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Binding Sites ; Crystallography, X-Ray ; DNA-Binding Proteins ; Dimerization ; Galactokinase/metabolism ; Galactose/metabolism ; Gene Expression Regulation, Fungal ; Models, Molecular ; NADP/*metabolism ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Recombinant Fusion Proteins/metabolism ; Repressor Proteins/*chemistry/genetics/*metabolism ; Saccharomyces cerevisiae/genetics/*metabolism ; Saccharomyces cerevisiae Proteins/*chemistry/genetics/*metabolism ; Transcription Factors/*chemistry/genetics/*metabolism ; Transcription, Genetic
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    Global protein stability profiling in mammalian cells (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-11-08
    Description: The abundance of cellular proteins is determined largely by the rate of transcription and translation coupled with the stability of individual proteins. Although we know a great deal about global transcript abundance, little is known about global protein stability. We present a highly parallel multiplexing strategy to monitor protein turnover on a global scale by coupling flow cytometry with microarray technology to track the stability of individual proteins within a complex mixture. We demonstrated the feasibility of this approach by measuring the stability of approximately 8000 human proteins and identifying proteasome substrates. The technology provides a general platform for proteome-scale analysis of protein turnover under various physiological and disease conditions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yen, Hsueh-Chi Sherry -- Xu, Qikai -- Chou, Danny M -- Zhao, Zhenming -- Elledge, Stephen J -- AG11085/AG/NIA NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Nov 7;322(5903):918-23. doi: 10.1126/science.1160489.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Center for Genetics and Genomics, Brigham and Women's Hospital, Howard Hughes Medical Institute, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18988847" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acids/analysis ; Cell Cycle ; Cell Line ; DNA, Complementary ; Flow Cytometry ; Green Fluorescent Proteins/analysis/metabolism ; Half-Life ; Humans ; Luminescent Proteins/analysis/metabolism ; Oligonucleotide Array Sequence Analysis ; Open Reading Frames ; Proteasome Endopeptidase Complex/*metabolism ; Protein Biosynthesis ; *Protein Stability ; Proteins/genetics/*metabolism ; RNA, Messenger/genetics/metabolism ; Recombinant Fusion Proteins/metabolism ; Transcription, Genetic
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    Molecular biology. Secret weapon (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-08-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Young, Ryland F 3rd -- New York, N.Y. -- Science. 2008 Aug 15;321(5891):922-3. doi: 10.1126/science.1162910.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, Texas A&M University, College Station, TX 77843-2128, USA. ryland@tamu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18703730" target="_blank"〉PubMed〈/a〉
    Keywords: Bacteriophage lambda/*genetics/*growth & development ; Cloning, Molecular ; DNA, Intergenic ; DNA, Viral ; Escherichia coli/*genetics/*virology ; Escherichia coli Proteins/genetics/*metabolism ; Genes, Bacterial ; Genome, Viral ; *Interspersed Repetitive Sequences ; RNA, Bacterial/*genetics/metabolism ; Ribonucleoproteins/metabolism ; Transcription, Genetic
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    Outwitting multidrug resistance to antifungals (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-07-19
    Description: The economic cost of fungal infection and its mortality associated with multidrug resistance remain unacceptably high. Recent understanding of the transcriptional regulation of plasma membrane efflux pumps of modest specificity provides new avenues for the development of broad-spectrum fungicides. Together with improved diagnosis and indirect intervention via inhibition of the energy supply for drug efflux, we envisage multifunctional azole analogs that inhibit not only ergosterol biosynthesis and drug efflux-pump activity but also activation of the transcriptional machinery that induces drug efflux-pump expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Monk, Brian C -- Goffeau, Andre -- DE016885/DE/NIDCR NIH HHS/ -- New York, N.Y. -- Science. 2008 Jul 18;321(5887):367-9. doi: 10.1126/science.1159746.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Oral Sciences, Faculty of Dentistry, University of Otago, Post Office Box 647, Dunedin, New Zealand.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18635793" target="_blank"〉PubMed〈/a〉
    Keywords: ATP-Binding Cassette Transporters/genetics/metabolism ; Antifungal Agents/metabolism/*pharmacology/therapeutic use ; *Drug Resistance, Multiple, Fungal/genetics ; Fungi/*drug effects/genetics/metabolism ; Gene Expression Regulation, Fungal ; Humans ; Membrane Transport Proteins/genetics/metabolism ; Mycoses/diagnosis/*drug therapy/*microbiology ; Transcription Factors/genetics/metabolism ; Transcription, Genetic
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    Structural insights into a circadian oscillator (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-11-01
    Description: An endogenous circadian system in cyanobacteria exerts pervasive control over cellular processes, including global gene expression. Indeed, the entire chromosome undergoes daily cycles of topological changes and compaction. The biochemical machinery underlying a circadian oscillator can be reconstituted in vitro with just three cyanobacterial proteins, KaiA, KaiB, and KaiC. These proteins interact to promote conformational changes and phosphorylation events that determine the phase of the in vitro oscillation. The high-resolution structures of these proteins suggest a ratcheting mechanism by which the KaiABC oscillator ticks unidirectionally. This posttranslational oscillator may interact with transcriptional and translational feedback loops to generate the emergent circadian behavior in vivo. The conjunction of structural, biophysical, and biochemical approaches to this system reveals molecular mechanisms of biological timekeeping.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2588432/" 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/PMC2588432/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Johnson, Carl Hirschie -- Egli, Martin -- Stewart, Phoebe L -- F32 GM71276/GM/NIGMS NIH HHS/ -- GM067152/GM/NIGMS NIH HHS/ -- GM073845/GM/NIGMS NIH HHS/ -- R01 GM067152/GM/NIGMS NIH HHS/ -- R01 GM067152-06/GM/NIGMS NIH HHS/ -- R01 GM073845/GM/NIGMS NIH HHS/ -- R01 GM073845-03/GM/NIGMS NIH HHS/ -- R01 MH043836/MH/NIMH NIH HHS/ -- R01 MH043836-17/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2008 Oct 31;322(5902):697-701. doi: 10.1126/science.1150451.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Box 35-1634, Vanderbilt University, Nashville, TN 37235-1634, USA. carl.h.johnson@vanderbilt.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18974343" target="_blank"〉PubMed〈/a〉
    Keywords: Bacterial Proteins/*chemistry/metabolism ; *Biological Clocks ; Cell Division ; Chromosomes, Bacterial/physiology ; *Circadian Rhythm ; Circadian Rhythm Signaling Peptides and Proteins ; Dimerization ; Models, Molecular ; Phosphorylation ; Promoter Regions, Genetic ; Protein Biosynthesis ; Protein Conformation ; Synechococcus/chemistry/genetics/*physiology ; Transcription, Genetic
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    Genetics. It's the sequence, stupid! (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-10-18
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4765165/" 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/PMC4765165/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Coller, Hilary A -- Kruglyak, Leonid -- R01 GM081686/GM/NIGMS NIH HHS/ -- R01 GM086465/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2008 Oct 17;322(5900):380-1. doi: 10.1126/science.1165664.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Princeton University, Princeton, NJ 08544, USA. hcoller@princeton.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18927376" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosomes, Human, Pair 21/*genetics/metabolism ; Disease Models, Animal ; Down Syndrome/genetics ; *Gene Expression Regulation ; Hepatocytes/*metabolism ; Histones/metabolism ; Humans ; Mice ; RNA, Messenger/genetics/metabolism ; *Regulatory Sequences, Nucleic Acid ; Species Specificity ; Transcription Factors/metabolism ; Transcription, Genetic
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    Signal transduction. Sweet conundrum (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-03-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Birnbaum, Morris J -- New York, N.Y. -- Science. 2008 Mar 7;319(5868):1348-9. doi: 10.1126/science.1155915.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Diabetes, Obesity and Metabolism, University of Pennsylvania, Philadelphia, PA 19104, USA. birnbaum@mail.med.upenn.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18323441" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Glucose/*metabolism ; Cell Nucleus/metabolism ; Cytoplasm/metabolism ; Diabetes Mellitus/metabolism ; Enzyme Activation ; Gene Expression Regulation ; Glucose/*metabolism ; Glucose-6-Phosphatase/genetics/metabolism ; Glycosylation ; Humans ; Insulin/metabolism ; Insulin Resistance ; Liver/*metabolism ; Mice ; Phosphorylation ; *Signal Transduction ; Trans-Activators/*metabolism ; Transcription Factors ; Transcription, Genetic ; Uridine Diphosphate N-Acetylglucosamine/metabolism
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  • 48
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    Deletional tolerance mediated by extrathymic Aire-expressing cells (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-08-09
    Description: The prevention of autoimmunity requires the elimination of self-reactive T cells during their development and maturation. The expression of diverse self-antigens by stromal cells in the thymus is essential to this process and depends, in part, on the activity of the autoimmune regulator (Aire) gene. Here we report the identification of extrathymic Aire-expressing cells (eTACs) resident within the secondary lymphoid organs. These stromally derived eTACs express a diverse array of distinct self-antigens and are capable of interacting with and deleting naive autoreactive T cells. Using two-photon microscopy, we observed stable antigen-specific interactions between eTACs and autoreactive T cells. We propose that such a secondary network of self-antigen-expressing stromal cells may help reinforce immune tolerance by preventing the maturation of autoreactive T cells that escape thymic negative selection.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2532844/" 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/PMC2532844/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gardner, James M -- Devoss, Jason J -- Friedman, Rachel S -- Wong, David J -- Tan, Ying X -- Zhou, Xuyu -- Johannes, Kellsey P -- Su, Maureen A -- Chang, Howard Y -- Krummel, Matthew F -- Anderson, Mark S -- K08 AI076429/AI/NIAID NIH HHS/ -- K08 AI076429-05/AI/NIAID NIH HHS/ -- P01 AI035297/AI/NIAID NIH HHS/ -- P01 AI035297-150009/AI/NIAID NIH HHS/ -- P01 AI035297-159001/AI/NIAID NIH HHS/ -- P01 AI035297-160009/AI/NIAID NIH HHS/ -- P01 AI035297-169001/AI/NIAID NIH HHS/ -- P01 AI035297-170009/AI/NIAID NIH HHS/ -- P01 AI035297-179001/AI/NIAID NIH HHS/ -- P30 DK063720/DK/NIDDK NIH HHS/ -- P30 DK063720-05/DK/NIDDK NIH HHS/ -- T32 GM007618/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2008 Aug 8;321(5890):843-7. doi: 10.1126/science.1159407.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Diabetes Center, University of California San Francisco (UCSF), San Francisco, CA 94122, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18687966" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; Antigen Presentation ; Autoantigens/genetics/*immunology ; Autoimmunity ; Cell Proliferation ; Epithelial Cells/immunology ; Gene Expression Regulation ; Glucose-6-Phosphatase/immunology ; Lymph Nodes/cytology/*immunology/metabolism ; Lymphoid Tissue/*cytology/immunology/*metabolism ; Mice ; Mice, Transgenic ; Proteins/immunology ; *Self Tolerance ; Spleen/cytology/immunology/metabolism ; Stromal Cells/immunology/metabolism ; T-Lymphocytes/*immunology ; Thymus Gland/cytology/immunology ; Transcription Factors/genetics/*metabolism ; Transcription, Genetic
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    Genomic plasticity and the diversity of polyploid plants (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-04-26
    Description: Polyploidy, a change whereby the entire chromosome set is multiplied, arises through mitotic or meiotic misdivisions and frequently involves unreduced gametes and interspecific hybridization. The success of newly formed angiosperm polyploids is partly attributable to their highly plastic genome structure, as manifested by tolerance to changing chromosome numbers (aneuploidy and polyploidy), genome size, (retro)transposable element mobility, insertions, deletions, and epigenome restructuring. The ability to withstand large-scale changes, frequently within one or a few generations, is associated with a restructuring of the transcriptome, metabolome, and proteome and can result in an altered phenotype and ecology. Thus, polyploid-induced changes can generate individuals that are able to exploit new niches or to outcompete progenitor species. This process has been a major driving force behind the divergence of the angiosperms and their biodiversity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leitch, A R -- Leitch, I J -- New York, N.Y. -- Science. 2008 Apr 25;320(5875):481-3. doi: 10.1126/science.1153585.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Biological and Chemical Sciences, Queen Mary, University of London, London E1 4NS, UK. a.r.leitch@qmul.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18436776" target="_blank"〉PubMed〈/a〉
    Keywords: Angiosperms/classification/*genetics/metabolism ; Biodiversity ; Biological Evolution ; Chromosomes, Plant/genetics ; Genetic Speciation ; *Genetic Variation ; *Genome, Plant ; Hybridization, Genetic ; Nondisjunction, Genetic ; Plant Proteins/genetics/metabolism ; *Polyploidy ; Proteome ; Transcription, Genetic
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    Chromatin-associated periodicity in genetic variation downstream of transcriptional start sites (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-12-17
    Description: Might DNA sequence variation reflect germline genetic activity and underlying chromatin structure? We investigated this question using medaka (Japanese killifish, Oryzias latipes), by comparing the genomic sequences of two strains (Hd-rR and HNI) and by mapping approximately 37.3 million nucleosome cores from Hd-rR blastulae and 11,654 representative transcription start sites from six embryonic stages. We observed a distinctive approximately 200-base pair (bp) periodic pattern of genetic variation downstream of transcription start sites; the rate of insertions and deletions longer than 1 bp peaked at positions of approximately +200, +400, and +600 bp, whereas the point mutation rate showed corresponding valleys. This approximately 200-bp periodicity was correlated with the chromatin structure, with nucleosome occupancy minimized at positions 0, +200, +400, and +600 bp. These data exemplify the potential for genetic activity (transcription) and chromatin structure to contribute to molding the DNA sequence on an evolutionary time scale.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2757552/" 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/PMC2757552/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sasaki, Shin -- Mello, Cecilia C -- Shimada, Atsuko -- Nakatani, Yoichiro -- Hashimoto, Shin-Ichi -- Ogawa, Masako -- Matsushima, Kouji -- Gu, Sam Guoping -- Kasahara, Masahiro -- Ahsan, Budrul -- Sasaki, Atsushi -- Saito, Taro -- Suzuki, Yutaka -- Sugano, Sumio -- Kohara, Yuji -- Takeda, Hiroyuki -- Fire, Andrew -- Morishita, Shinichi -- R01 GM037706/GM/NIGMS NIH HHS/ -- R01 GM037706-24/GM/NIGMS NIH HHS/ -- R01 GM37706/GM/NIGMS NIH HHS/ -- T32 CA009151/CA/NCI NIH HHS/ -- T32 CA09151/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2009 Jan 16;323(5912):401-4. doi: 10.1126/science.1163183. Epub 2008 Dec 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Computational Biology, Graduate School of Frontier Sciences, University of Tokyo, Kashiwa, 277-0882, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19074313" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Composition ; Base Sequence ; Chromatin/*physiology/ultrastructure ; DNA/chemistry/*genetics ; DNA Repair ; *Genetic Variation ; Genome ; INDEL Mutation ; Mutagenesis ; Mutation ; Nucleosomes/*physiology/ultrastructure ; Oryzias/embryology/*genetics ; Point Mutation ; Promoter Regions, Genetic ; *Transcription Initiation Site ; Transcription, Genetic
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Human fetal hemoglobin expression is regulated by the developmental stage-specific repressor BCL11A (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-12-06
    Description: Differences in the amount of fetal hemoglobin (HbF) that persists into adulthood affect the severity of sickle cell disease and the beta-thalassemia syndromes. Genetic association studies have identified sequence variants in the gene BCL11A that influence HbF levels. Here, we examine BCL11A as a potential regulator of HbF expression. The high-HbF BCL11A genotype is associated with reduced BCL11A expression. Moreover, abundant expression of full-length forms of BCL11A is developmentally restricted to adult erythroid cells. Down-regulation of BCL11A expression in primary adult erythroid cells leads to robust HbF expression. Consistent with a direct role of BCL11A in globin gene regulation, we find that BCL11A occupies several discrete sites in the beta-globin gene cluster. BCL11A emerges as a therapeutic target for reactivation of HbF in beta-hemoglobin disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sankaran, Vijay G -- Menne, Tobias F -- Xu, Jian -- Akie, Thomas E -- Lettre, Guillaume -- Van Handel, Ben -- Mikkola, Hanna K A -- Hirschhorn, Joel N -- Cantor, Alan B -- Orkin, Stuart H -- HL32259-27/HL/NHLBI NIH HHS/ -- HL32262-26/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Dec 19;322(5909):1839-42. doi: 10.1126/science.1165409. Epub 2008 Dec 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematology/Oncology, Children's Hospital Boston, Harvard Stem Cell Institute, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19056937" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carrier Proteins/*genetics/metabolism ; Cell Line, Tumor ; Cells, Cultured ; Down-Regulation ; Erythroblasts/metabolism ; Erythroid Cells/*metabolism ; Erythroid Precursor Cells/metabolism ; Erythropoiesis ; Fetal Hemoglobin/biosynthesis/*genetics ; GATA1 Transcription Factor/metabolism ; *Gene Expression Regulation ; Hemoglobinopathies/therapy ; Histone Deacetylases/metabolism ; Humans ; K562 Cells ; Mi-2 Nucleosome Remodeling and Deacetylase Complex ; Mice ; Multigene Family ; Nuclear Proteins/*genetics/metabolism ; Polymorphism, Single Nucleotide ; Protein Isoforms/genetics/metabolism ; RNA Interference ; Transcription Factors/metabolism ; Transcription, Genetic ; beta-Globins/genetics/metabolism ; gamma-Globins/genetics/metabolism
    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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    Small CRISPR RNAs guide antiviral defense in prokaryotes (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-08-16
    Description: Prokaryotes acquire virus resistance by integrating short fragments of viral nucleic acid into clusters of regularly interspaced short palindromic repeats (CRISPRs). Here we show how virus-derived sequences contained in CRISPRs are used by CRISPR-associated (Cas) proteins from the host to mediate an antiviral response that counteracts infection. After transcription of the CRISPR, a complex of Cas proteins termed Cascade cleaves a CRISPR RNA precursor in each repeat and retains the cleavage products containing the virus-derived sequence. Assisted by the helicase Cas3, these mature CRISPR RNAs then serve as small guide RNAs that enable Cascade to interfere with virus proliferation. Our results demonstrate that the formation of mature guide RNAs by the CRISPR RNA endonuclease subunit of Cascade is a mechanistic requirement for antiviral defense.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brouns, Stan J J -- Jore, Matthijs M -- Lundgren, Magnus -- Westra, Edze R -- Slijkhuis, Rik J H -- Snijders, Ambrosius P L -- Dickman, Mark J -- Makarova, Kira S -- Koonin, Eugene V -- van der Oost, John -- New York, N.Y. -- Science. 2008 Aug 15;321(5891):960-4. doi: 10.1126/science.1159689.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Microbiology, Department of Agrotechnology and Food Sciences, Wageningen University, Dreijenplein 10, 6703 HB Wageningen, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18703739" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Bacteriophage lambda/*genetics/*growth & development ; Base Sequence ; DNA, Intergenic ; DNA, Viral/metabolism ; Escherichia coli/genetics/metabolism ; Escherichia coli K12/*genetics/metabolism/*virology ; Escherichia coli Proteins/chemistry/genetics/*metabolism ; Genes, Bacterial ; Molecular Sequence Data ; RNA Precursors/metabolism ; RNA, Bacterial/*genetics/metabolism ; RNA, Guide/genetics/metabolism ; *Repetitive Sequences, Nucleic Acid ; Transcription, Genetic ; Viral Plaque Assay
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    Identification of host proteins required for HIV infection through a functional genomic screen (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-01-12
    Description: HIV-1 exploits multiple host proteins during infection. We performed a large-scale small interfering RNA screen to identify host factors required by HIV-1 and identified more than 250 HIV-dependency factors (HDFs). These proteins participate in a broad array of cellular functions and implicate new pathways in the viral life cycle. Further analysis revealed previously unknown roles for retrograde Golgi transport proteins (Rab6 and Vps53) in viral entry, a karyopherin (TNPO3) in viral integration, and the Mediator complex (Med28) in viral transcription. Transcriptional analysis revealed that HDF genes were enriched for high expression in immune cells, suggesting that viruses evolve in host cells that optimally perform the functions required for their life cycle. This effort illustrates the power with which RNA interference and forward genetics can be used to expose the dependencies of human pathogens such as HIV, and in so doing identify potential targets for therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brass, Abraham L -- Dykxhoorn, Derek M -- Benita, Yair -- Yan, Nan -- Engelman, Alan -- Xavier, Ramnik J -- Lieberman, Judy -- Elledge, Stephen J -- AI052014/AI/NIAID NIH HHS/ -- AI062773/AI/NIAID NIH HHS/ -- P30 AI060354/AI/NIAID NIH HHS/ -- P30 DK040561/DK/NIDDK NIH HHS/ -- P30 DK040561-13/DK/NIDDK NIH HHS/ -- U19-AI056900/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Feb 15;319(5865):921-6. doi: 10.1126/science.1152725. Epub 2008 Jan 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Center for Genetics and Genomics, Brigham and Women's Hospital, Howard Hughes Medical Institute, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18187620" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line, Tumor ; Computational Biology ; Cytoskeletal Proteins/genetics/physiology ; Genomics ; HIV Infections/genetics/metabolism/*virology ; HIV-1/genetics/pathogenicity/*physiology ; Host-Pathogen Interactions ; Human Immunodeficiency Virus Proteins/physiology ; Humans ; Intracellular Signaling Peptides and Proteins/genetics/physiology ; Karyopherins/genetics/physiology ; Mediator Complex ; Proteins/*physiology ; RNA Interference ; RNA, Small Interfering ; Transcription, Genetic ; Vesicular Transport Proteins/genetics/physiology ; Virus Integration ; Virus Internalization ; Virus Replication ; rab GTP-Binding Proteins/genetics/physiology
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    Plastin 3 is a protective modifier of autosomal recessive spinal muscular atrophy (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-04-29
    Description: Homozygous deletion of the survival motor neuron 1 gene (SMN1) causes spinal muscular atrophy (SMA), the most frequent genetic cause of early childhood lethality. In rare instances, however, individuals are asymptomatic despite carrying the same SMN1 mutations as their affected siblings, thereby suggesting the influence of modifier genes. We discovered that unaffected SMN1-deleted females exhibit significantly higher expression of plastin 3 (PLS3) than their SMA-affected counterparts. We demonstrated that PLS3 is important for axonogenesis through increasing the F-actin level. Overexpression of PLS3 rescued the axon length and outgrowth defects associated with SMN down-regulation in motor neurons of SMA mouse embryos and in zebrafish. Our study suggests that defects in axonogenesis are the major cause of SMA, thereby opening new therapeutic options for SMA and similar neuromuscular diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oprea, Gabriela E -- Krober, Sandra -- McWhorter, Michelle L -- Rossoll, Wilfried -- Muller, Stefan -- Krawczak, Michael -- Bassell, Gary J -- Beattie, Christine E -- Wirth, Brunhilde -- HD055835/HD/NICHD NIH HHS/ -- R01 HD055835/HD/NICHD NIH HHS/ -- R01NS50414/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2008 Apr 25;320(5875):524-7. doi: 10.1126/science.1155085.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Human Genetics, University of Cologne, 50931 Cologne, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18440926" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/blood/*genetics/*metabolism ; Animals ; Axons/metabolism/*physiology/ultrastructure ; Cell Differentiation ; Cell Line ; Cyclic AMP Response Element-Binding Protein/genetics/metabolism ; Female ; Gene Expression ; Growth Cones/metabolism/ultrastructure ; Humans ; Male ; Membrane Glycoproteins ; Mice ; Microfilament Proteins ; Muscular Atrophy, Spinal/*genetics ; Nerve Tissue Proteins/genetics/metabolism ; Pedigree ; Phosphoproteins/blood/*genetics/*metabolism ; RNA-Binding Proteins/genetics/metabolism ; SMN Complex Proteins ; Spinal Cord/metabolism ; Survival of Motor Neuron 1 Protein ; Transcription, Genetic ; Zebrafish/embryology/genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Multilevel regulation of gene expression by microRNAs (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-03-29
    Description: MicroRNAs (miRNAs) are approximately 22-nucleotide-long noncoding RNAs that normally function by suppressing translation and destabilizing messenger RNAs bearing complementary target sequences. Some miRNAs are expressed in a cell- or tissue-specific manner and may contribute to the establishment and/or maintenance of cellular identity. Recent studies indicate that tissue-specific miRNAs may function at multiple hierarchical levels of gene regulatory networks, from targeting hundreds of effector genes incompatible with the differentiated state to controlling the levels of global regulators of transcription and alternative pre-mRNA splicing. This multilevel regulation may allow individual miRNAs to profoundly affect the gene expression program of differentiated cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3139454/" 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/PMC3139454/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Makeyev, Eugene V -- Maniatis, Tom -- 2R01NS043915-27/NS/NINDS NIH HHS/ -- R01 NS043915/NS/NINDS NIH HHS/ -- R01 NS043915-27/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2008 Mar 28;319(5871):1789-90. doi: 10.1126/science.1152326.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA. makeyev@mcb.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18369137" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Animals ; Cell Differentiation ; *Gene Expression Regulation ; Gene Regulatory Networks ; Humans ; MicroRNAs/*genetics/metabolism ; Muscle Cells/cytology/metabolism ; Neurons/cytology/metabolism ; Transcription Factors/metabolism ; Transcription, Genetic
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    Circadian rhythms. Integrating circadian timekeeping with cellular physiology (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-05-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Harrisingh, Marie C -- Nitabach, Michael N -- New York, N.Y. -- Science. 2008 May 16;320(5878):879-80. doi: 10.1126/science.1158619.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Physiology, Yale School of Medicine, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18487177" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arabidopsis/genetics/physiology ; Biological Clocks/genetics/*physiology ; CLOCK Proteins ; Calcium/metabolism ; *Calcium Signaling ; Circadian Rhythm/genetics/*physiology ; Cyclic ADP-Ribose/*metabolism ; Cyclic AMP/*metabolism ; Cyclic AMP Response Element-Binding Protein/metabolism ; Drosophila melanogaster/genetics/physiology ; Feedback, Physiological ; Gene Expression Regulation ; Mice ; Signal Transduction ; Suprachiasmatic Nucleus/*physiology ; Trans-Activators/*genetics ; Transcription, Genetic
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    Chromosome alignment and transvection are antagonized by condensin II (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-11-29
    Description: Polytene chromosome structure is a characteristic of some polyploid cells where several to thousands of chromatids are closely associated with perfect alignment of homologous DNA sequences. Here, we show that Drosophila condensin II promotes disassembly of polytene structure into chromosomal components. Condensin II also negatively regulates transvection, a process whereby certain alleles are influenced transcriptionally via interallelic physical associations. We propose that condensin II restricts trans-chromosomal interactions that affect transcription through its ability to spatially separate aligned interphase chromosomes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hartl, Tom A -- Smith, Helen F -- Bosco, Giovanni -- GM069462/GM/NIGMS NIH HHS/ -- R01 GM069462/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2008 Nov 28;322(5906):1384-7. doi: 10.1126/science.1164216.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, University of Arizona, 1007 East Lowell Street, Tucson, AZ 85721-0106, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19039137" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphatases/genetics/*metabolism ; Alleles ; Animals ; Cell Cycle ; Chromosomes/genetics/*physiology/ultrastructure ; DNA-Binding Proteins/genetics/*metabolism ; Drosophila Proteins/genetics/*metabolism/physiology ; Drosophila melanogaster/*genetics/growth & development ; Gene Expression Regulation ; Genes, Insect ; Homeodomain Proteins/genetics/physiology ; Interphase ; Larva/genetics ; Multiprotein Complexes/genetics/*metabolism ; Mutant Proteins/metabolism ; Pigmentation/genetics ; Salivary Glands ; Transcription Factors/genetics/physiology ; Transcription, Genetic
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    Cell identity mediates the response of Arabidopsis roots to abiotic stress (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-04-26
    Description: Little is known about the way developmental cues affect how cells interpret their environment. We characterized the transcriptional response to high salinity of different cell layers and developmental stages of the Arabidopsis root and found that transcriptional responses are highly constrained by developmental parameters. These transcriptional changes lead to the differential regulation of specific biological functions in subsets of cell layers, several of which correspond to observable physiological changes. We showed that known stress pathways primarily control semiubiquitous responses and used mutants that disrupt epidermal patterning to reveal cell-layer-specific and inter-cell-layer effects. By performing a similar analysis using iron deprivation, we identified common cell-type-specific stress responses and revealed the crucial role the environment plays in defining the transcriptional outcome of cell-fate decisions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dinneny, Jose R -- Long, Terri A -- Wang, Jean Y -- Jung, Jee W -- Mace, Daniel -- Pointer, Solomon -- Barron, Christa -- Brady, Siobhan M -- Schiefelbein, John -- Benfey, Philip N -- New York, N.Y. -- Science. 2008 May 16;320(5878):942-5. doi: 10.1126/science.1153795. Epub 2008 Apr 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Duke University, Durham, NC 27708, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18436742" target="_blank"〉PubMed〈/a〉
    Keywords: Abscisic Acid/metabolism ; Algorithms ; Arabidopsis/*cytology/genetics/*physiology ; Arabidopsis Proteins/genetics/metabolism ; Culture Media ; Gene Expression Profiling ; *Gene Expression Regulation, Plant ; Genes, Plant ; Iron/metabolism ; Mutation ; Plant Epidermis/cytology/genetics/physiology ; Plant Roots/*cytology/genetics/growth & development/*physiology ; Promoter Regions, Genetic ; Response Elements ; *Salinity ; Transcription Factors/metabolism ; Transcription, Genetic
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    The eukaryotic genome as an RNA machine (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-03-29
    Description: The past few years have revealed that the genomes of all studied eukaryotes are almost entirely transcribed, generating an enormous number of non-protein-coding RNAs (ncRNAs). In parallel, it is increasingly evident that many of these RNAs have regulatory functions. Here, we highlight recent advances that illustrate the diversity of ncRNA control of genome dynamics, cell biology, and developmental programming.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Amaral, Paulo P -- Dinger, Marcel E -- Mercer, Tim R -- Mattick, John S -- New York, N.Y. -- Science. 2008 Mar 28;319(5871):1787-9. doi: 10.1126/science.1155472.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Molecular Bioscience, University of Queensland, St. Lucia QLD 4072, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18369136" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Eukaryotic Cells/*metabolism ; Evolution, Molecular ; *Gene Expression Regulation ; Genome ; Genome, Human ; Humans ; Protein Biosynthesis ; RNA Processing, Post-Transcriptional ; RNA, Untranslated/*genetics/metabolism ; Transcription, Genetic
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    Molecular biology. The paradox of silent heterochromatin (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-05-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Djupedal, Ingela -- Ekwall, Karl -- New York, N.Y. -- Science. 2008 May 2;320(5876):624-5. doi: 10.1126/science.1158923.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biosciences and Medical Nutrition, Karolinska Institutet, Sweden/School of Life Sciences, University College Sodertorn, NOVUM, 141 57 Huddinge, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18451292" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Cycle/genetics ; Heterochromatin/*physiology ; Models, Biological ; RNA Interference ; RNA Polymerase II/metabolism ; RNA, Fungal/physiology ; Schizosaccharomyces/genetics/physiology ; Transcription, Genetic
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    Glia are essential for sensory organ function in C. elegans (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-11-01
    Description: Sensory organs are composed of neurons, which convert environmental stimuli to electrical signals, and glia-like cells, whose functions are not well understood. To decipher glial roles in sensory organs, we ablated the sheath glial cell of the major sensory organ of Caenorhabditis elegans. We found that glia-ablated animals exhibit profound sensory deficits and that glia provide activities that affect neuronal morphology, behavior generation, and neuronal uptake of lipophilic dyes. To understand the molecular bases of these activities, we identified 298 genes whose messenger RNAs are glia-enriched. One gene, fig-1, encodes a labile protein with conserved thrombospondin TSP1 domains. FIG-1 protein functions extracellularly, is essential for neuronal dye uptake, and also affects behavior. Our results suggest that glia are required for multiple aspects of sensory organ function.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2735448/" 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/PMC2735448/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bacaj, Taulant -- Tevlin, Maya -- Lu, Yun -- Shaham, Shai -- R01 NS064273/NS/NINDS NIH HHS/ -- R01 NS064273-01/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2008 Oct 31;322(5902):744-7. doi: 10.1126/science.1163074.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Developmental Genetics, Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18974354" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/cytology/genetics/*physiology ; Caenorhabditis elegans Proteins/analysis/chemistry/genetics/*physiology ; Calcium/metabolism ; Carbocyanines/metabolism ; Chemotaxis ; Cilia/chemistry/ultrastructure ; Fluorescent Dyes/metabolism ; Gene Expression ; Genes, Helminth ; Neuroglia/*physiology ; Odors ; Oligonucleotide Array Sequence Analysis ; Osmolar Concentration ; Sense Organs/physiology ; Sensory Receptor Cells/cytology/*physiology ; Signal Transduction ; Sodium Chloride ; Temperature ; Thrombospondins/chemistry/genetics/*physiology ; Transcription, Genetic
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    Genome-scale proteomics reveals Arabidopsis thaliana gene models and proteome dynamics (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-04-26
    Description: We have assembled a proteome map for Arabidopsis thaliana from high-density, organ-specific proteome catalogs that we generated for different organs, developmental stages, and undifferentiated cultured cells. We matched 86,456 unique peptides to 13,029 proteins and provide expression evidence for 57 gene models that are not represented in the TAIR7 protein database. Analysis of the proteome identified organ-specific biomarkers and allowed us to compile an organ-specific set of proteotypic peptides for 4105 proteins to facilitate targeted quantitative proteomics surveys. Quantitative information for the identified proteins was used to establish correlations between transcript and protein accumulation in different plant organs. The Arabidopsis proteome map provides information about genome activity and proteome assembly and is available as a resource for plant systems biology.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baerenfaller, Katja -- Grossmann, Jonas -- Grobei, Monica A -- Hull, Roger -- Hirsch-Hoffmann, Matthias -- Yalovsky, Shaul -- Zimmermann, Philip -- Grossniklaus, Ueli -- Gruissem, Wilhelm -- Baginsky, Sacha -- New York, N.Y. -- Science. 2008 May 16;320(5878):938-41. doi: 10.1126/science.1157956. Epub 2008 Apr 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Plant Sciences, ETH (Swiss Federal Institute of Technology) Zurich, Universitatstrasse 2, 8092 Zurich, Switzerland. kbaerenfaller@ethz.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18436743" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Amino Acid Sequence ; Arabidopsis/*chemistry/cytology/*genetics/physiology ; Arabidopsis Proteins/*analysis/chemistry/genetics ; Base Sequence ; Biomarkers/analysis ; Cells, Cultured ; Computational Biology ; Databases, Genetic ; Flowers/chemistry/genetics ; Gene Expression Profiling ; Gene Expression Regulation, Plant ; *Genome, Plant ; Models, Genetic ; Molecular Sequence Data ; Peptides/analysis/chemistry ; Plant Roots/chemistry/genetics ; Proteome/*analysis ; *Proteomics ; Seeds/chemistry/genetics ; Transcription, Genetic
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    Developmental biology. From genetic association to genetic switch (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-12-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Michelson, Alan M -- New York, N.Y. -- Science. 2008 Dec 19;322(5909):1803-4. doi: 10.1126/science.1169216.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Heart, Lung and Blood Institute, National Institutes of Health, 31 Center Drive, Bethesda, MD 20892, USA. michelsonam@mail.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19095932" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Carrier Proteins/*genetics/metabolism ; Cell Line ; Erythroid Cells/*metabolism ; Erythropoiesis ; Fetal Hemoglobin/biosynthesis/*genetics ; *Gene Expression Regulation ; Genome, Human ; *Genome-Wide Association Study ; Hemoglobinopathies/therapy ; Humans ; Introns ; Nuclear Proteins/*genetics/metabolism ; Polymorphism, Single Nucleotide ; Transcription, Genetic ; beta-Globins/genetics ; gamma-Globins/*genetics
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    Activation of FOXO1 by Cdk1 in cycling cells and postmitotic neurons (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-03-22
    Description: Activation of cyclin-dependent kinase 1 (Cdk1) has been linked to cell death of postmitotic neurons in brain development and disease. We found that Cdk1 phosphorylated the transcription factor FOXO1 at Ser249 in vitro and in vivo. The phosphorylation of FOXO1 at Ser249 disrupted FOXO1 binding with 14-3-3 proteins and thereby promoted the nuclear accumulation of FOXO1 and stimulated FOXO1-dependent transcription, leading to cell death in neurons. In proliferating cells, Cdk1 induced FOXO1 Ser249 phosphorylation at the G2/M phase of the cell cycle, resulting in FOXO1-dependent expression of the mitotic regulator Polo-like kinase (Plk). These findings define a conserved signaling link between Cdk1 and FOXO1 that may have a key role in diverse biological processes, including the degeneration of postmitotic neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yuan, Zengqiang -- Becker, Esther B E -- Merlo, Paola -- Yamada, Tomoko -- DiBacco, Sara -- Konishi, Yoshiyuki -- Schaefer, Erik M -- Bonni, Azad -- NS047188/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2008 Mar 21;319(5870):1665-8. doi: 10.1126/science.1152337.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18356527" target="_blank"〉PubMed〈/a〉
    Keywords: 14-3-3 Proteins/metabolism ; Animals ; Apoptosis ; CDC2 Protein Kinase/*metabolism ; *Cell Cycle ; Cell Cycle Proteins/genetics/metabolism ; Cell Line, Tumor ; Cell Nucleus/metabolism ; Cell Proliferation ; Cells, Cultured ; Forkhead Transcription Factors/*metabolism ; Humans ; Mice ; NIH 3T3 Cells ; Nerve Tissue Proteins/*metabolism ; Neurons/cytology/*metabolism ; Phosphorylation ; Protein-Serine-Threonine Kinases/genetics/metabolism ; Proto-Oncogene Proteins/genetics/metabolism ; Rats ; Serine/metabolism ; Signal Transduction ; Transcription, Genetic
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    Multiple high-throughput analyses monitor the response of E. coli to perturbations (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-03-24
    Description: Analysis of cellular components at multiple levels of biological information can provide valuable functional insights. We performed multiple high-throughput measurements to study the response of Escherichia coli cells to genetic and environmental perturbations. Analysis of metabolic enzyme gene disruptants revealed unexpectedly small changes in messenger RNA and proteins for most disruptants. Overall, metabolite levels were also stable, reflecting the rerouting of fluxes in the metabolic network. In contrast, E. coli actively regulated enzyme levels to maintain a stable metabolic state in response to changes in growth rate. E. coli thus seems to use complementary strategies that result in a metabolic network robust against perturbations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ishii, Nobuyoshi -- Nakahigashi, Kenji -- Baba, Tomoya -- Robert, Martin -- Soga, Tomoyoshi -- Kanai, Akio -- Hirasawa, Takashi -- Naba, Miki -- Hirai, Kenta -- Hoque, Aminul -- Ho, Pei Yee -- Kakazu, Yuji -- Sugawara, Kaori -- Igarashi, Saori -- Harada, Satoshi -- Masuda, Takeshi -- Sugiyama, Naoyuki -- Togashi, Takashi -- Hasegawa, Miki -- Takai, Yuki -- Yugi, Katsuyuki -- Arakawa, Kazuharu -- Iwata, Nayuta -- Toya, Yoshihiro -- Nakayama, Yoichi -- Nishioka, Takaaki -- Shimizu, Kazuyuki -- Mori, Hirotada -- Tomita, Masaru -- New York, N.Y. -- Science. 2007 Apr 27;316(5824):593-7. Epub 2007 Mar 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Advanced Biosciences, Keio University, Tsuruoka, Yamagata 997-0017, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17379776" target="_blank"〉PubMed〈/a〉
    Keywords: Chromatography, Liquid ; Computational Biology ; Electrophoresis, Capillary ; Electrophoresis, Gel, Two-Dimensional ; Enzyme Induction ; Enzyme Repression ; Enzymes/genetics/metabolism ; Escherichia coli/enzymology/*genetics/growth & development/*metabolism ; Escherichia coli Proteins/genetics/*metabolism ; Gene Expression ; *Genes, Bacterial ; Mass Spectrometry ; *Metabolic Networks and Pathways/genetics ; Mutation ; Oligonucleotide Array Sequence Analysis ; Proteome ; RNA, Messenger/genetics/metabolism ; Systems Biology/*methods ; Transcription, Genetic
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    Cell signaling. A ciliary signaling switch (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-07-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Christensen, Soren Tvorup -- Ott, Carolyn Marie -- New York, N.Y. -- Science. 2007 Jul 20;317(5836):330-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, University of Copenhagen, Copenhagen DK-2100, Denmark. stchristensen@aki.ku.dk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17641189" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Membrane/metabolism ; Cilia/*physiology ; Hedgehog Proteins/*metabolism ; Kruppel-Like Transcription Factors/metabolism ; Mice ; Receptors, Cell Surface/*metabolism ; Receptors, G-Protein-Coupled/metabolism ; *Signal Transduction ; Sterols/metabolism ; Transcription, Genetic
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    Widespread role for the flowering-time regulators FCA and FPA in RNA-mediated chromatin silencing (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-10-06
    Description: The RRM-domain proteins FCA and FPA have previously been characterized as flowering-time regulators in Arabidopsis. We show that they are required for RNA-mediated chromatin silencing of a range of loci in the genome. At some target loci, FCA and FPA promote asymmetric DNA methylation, whereas at others they function in parallel to DNA methylation. Female gametophytic development and early embryonic development are particularly susceptible to malfunctions in FCA and FPA. We propose that FCA and FPA regulate chromatin silencing of single and low-copy genes and interact in a locus-dependent manner with the canonical small interfering RNA-directed DNA methylation pathway to regulate common targets.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baurle, Isabel -- Smith, Lisa -- Baulcombe, David C -- Dean, Caroline -- New York, N.Y. -- Science. 2007 Oct 5;318(5847):109-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Developmental Biology, John Innes Centre, Norwich NR4 7UH, UK. isabel.baurle@bbsrc.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17916737" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/*genetics/growth & development/metabolism ; Arabidopsis Proteins/chemistry/genetics/*metabolism ; Chromatin/*genetics ; DNA Methylation ; DNA Transposable Elements ; DNA, Plant/metabolism ; Flowers/growth & development ; Mutation ; Oxidoreductases/genetics ; *RNA Interference ; RNA, Plant/genetics ; RNA, Small Interfering/genetics ; RNA-Binding Proteins/chemistry/genetics/*metabolism ; Retroelements ; Transcription, Genetic
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    Genome-wide mapping of in vivo protein-DNA interactions (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-06-02
    Description: In vivo protein-DNA interactions connect each transcription factor with its direct targets to form a gene network scaffold. To map these protein-DNA interactions comprehensively across entire mammalian genomes, we developed a large-scale chromatin immunoprecipitation assay (ChIPSeq) based on direct ultrahigh-throughput DNA sequencing. This sequence census method was then used to map in vivo binding of the neuron-restrictive silencer factor (NRSF; also known as REST, for repressor element-1 silencing transcription factor) to 1946 locations in the human genome. The data display sharp resolution of binding position [+/-50 base pairs (bp)], which facilitated our finding motifs and allowed us to identify noncanonical NRSF-binding motifs. These ChIPSeq data also have high sensitivity and specificity [ROC (receiver operator characteristic) area 〉/= 0.96] and statistical confidence (P 〈10(-4)), properties that were important for inferring new candidate interactions. These include key transcription factors in the gene network that regulates pancreatic islet cell development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Johnson, David S -- Mortazavi, Ali -- Myers, Richard M -- Wold, Barbara -- 5T32GM07616/GM/NIGMS NIH HHS/ -- U01 HG003162/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2007 Jun 8;316(5830):1497-502. Epub 2007 May 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Stanford University School of Medicine, Stanford, CA, 94305-5120, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17540862" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Amino Acid Motifs ; Binding Sites ; *Chromatin Immunoprecipitation ; DNA/*metabolism ; DNA-Binding Proteins/chemistry/*metabolism ; Gene Regulatory Networks ; *Genome, Human ; Humans ; Insulin-Secreting Cells/cytology/physiology ; MicroRNAs/genetics ; Neurons/physiology ; Promoter Regions, Genetic ; Protein Binding ; Repressor Proteins/chemistry/genetics/*metabolism ; Sensitivity and Specificity ; *Sequence Analysis, DNA ; Synaptic Transmission ; T-Lymphocytes/metabolism ; Transcription Factors/chemistry/genetics/*metabolism ; Transcription, Genetic ; Zinc Fingers
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    Staphylococcus aureus Panton-Valentine leukocidin causes necrotizing pneumonia (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-01-20
    Description: The Staphylococcus aureus Panton-Valentine leukocidin (PVL) is a pore-forming toxin secreted by strains epidemiologically associated with the current outbreak of community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) and with the often-lethal necrotizing pneumonia. To investigate the role of PVL in pulmonary disease, we tested the pathogenicity of clinical isolates, isogenic PVL-negative and PVL-positive S. aureus strains, as well as purified PVL, in a mouse acute pneumonia model. Here we show that PVL is sufficient to cause pneumonia and that the expression of this leukotoxin induces global changes in transcriptional levels of genes encoding secreted and cell wall-anchored staphylococcal proteins, including the lung inflammatory factor staphylococcal protein A (Spa).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Labandeira-Rey, Maria -- Couzon, Florence -- Boisset, Sandrine -- Brown, Eric L -- Bes, Michele -- Benito, Yvonne -- Barbu, Elena M -- Vazquez, Vanessa -- Hook, Magnus -- Etienne, Jerome -- Vandenesch, Francois -- Bowden, M Gabriela -- AI020624/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2007 Feb 23;315(5815):1130-3. Epub 2007 Jan 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Extracellular Matrix Biology, Institute of Biosciences and Technology, Texas A&M University System Health Science Center, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17234914" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Proteins/genetics/metabolism ; Bacterial Toxins/genetics ; Calcium-Binding Proteins/genetics/metabolism ; Disease Models, Animal ; Exotoxins/genetics/*physiology ; Gene Expression Profiling ; Gene Expression Regulation, Bacterial ; Hemorrhage ; Leukocidins/genetics/*physiology ; Lung/microbiology/*pathology ; Methicillin Resistance ; Mice ; Mice, Inbred BALB C ; Necrosis ; Oligonucleotide Array Sequence Analysis ; Pneumonia, Staphylococcal/*microbiology/*pathology ; Staphylococcal Protein A/genetics/*metabolism ; Staphylococcus aureus/genetics/growth & development/metabolism/*pathogenicity ; Transcription, Genetic ; Virulence ; Virulence Factors/genetics/*physiology
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    Permuted tRNA genes expressed via a circular RNA intermediate in Cyanidioschyzon merolae (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-10-20
    Description: A computational analysis of the nuclear genome of a red alga, Cyanidioschyzon merolae, identified 11 transfer RNA (tRNA) genes in which the 3' half of the tRNA lies upstream of the 5' half in the genome. We verified that these genes are expressed and produce mature tRNAs that are aminoacylated. Analysis of tRNA-processing intermediates for these genes indicates an unusual processing pathway in which the termini of the tRNA precursor are ligated, resulting in formation of a characteristic circular RNA intermediate that is then processed at the acceptor stem to generate the correct termini.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Soma, Akiko -- Onodera, Akinori -- Sugahara, Junichi -- Kanai, Akio -- Yachie, Nozomu -- Tomita, Masaru -- Kawamura, Fujio -- Sekine, Yasuhiko -- New York, N.Y. -- Science. 2007 Oct 19;318(5849):450-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Life Science, College of Science, Rikkyo (St. Paul's) University, Toshima, Tokyo 171-8501, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17947580" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; DNA, Algal/chemistry/genetics ; *Genes ; Methionine-tRNA Ligase/metabolism ; Molecular Sequence Data ; Nucleic Acid Conformation ; RNA/chemistry/genetics/*metabolism ; RNA Processing, Post-Transcriptional ; RNA, Algal/*genetics/metabolism ; RNA, Transfer/*genetics/metabolism ; RNA, Transfer, Amino Acyl/metabolism ; Rhodophyta/*genetics/metabolism ; Transcription, Genetic
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    Genetic properties influencing the evolvability of gene expression (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-05-26
    Description: Identifying the properties of gene networks that influence their evolution is a fundamental research goal. However, modes of evolution cannot be inferred solely from the distribution of natural variation, because selection interacts with demography and mutation rates to shape polymorphism and divergence. We estimated the effects of naturally occurring mutations on gene expression while minimizing the effect of natural selection. We demonstrate that sensitivity of gene expression to mutations increases with both increasing trans-mutational target size and the presence of a TATA box. Genes with greater sensitivity to mutations are also more sensitive to systematic environmental perturbations and stochastic noise. These results provide a mechanistic basis for gene expression evolvability that can serve as a foundation for realistic models of regulatory evolution.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Landry, Christian R -- Lemos, Bernardo -- Rifkin, Scott A -- Dickinson, W J -- Hartl, Daniel L -- New York, N.Y. -- Science. 2007 Jul 6;317(5834):118-21. Epub 2007 May 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Organismic and Evolutionary Biology, Harvard University, 16 Divinity Avenue, Cambridge, MA 02138, USA. clandry@post.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17525304" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites ; *Evolution, Molecular ; *Gene Expression ; Gene Expression Regulation, Fungal ; *Gene Regulatory Networks ; *Genes, Fungal ; Genetic Variation ; Linear Models ; Models, Genetic ; *Mutation ; Oligonucleotide Array Sequence Analysis ; Phenotype ; Promoter Regions, Genetic ; Saccharomyces cerevisiae/*genetics ; Selection, Genetic ; TATA Box ; Transcription Factors/metabolism ; Transcription, Genetic
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    Demethylation of H3K27 regulates polycomb recruitment and H2A ubiquitination (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-09-01
    Description: Methylation of histone H3 lysine 27 (H3K27) is a posttranslational modification that is highly correlated with genomic silencing. Here we show that human UTX, a member of the Jumonji C family of proteins, is a di- and trimethyl H3K27 demethylase. UTX occupies the promoters of HOX gene clusters and regulates their transcriptional output by modulating the recruitment of polycomb repressive complex 1 and the monoubiquitination of histone H2A. Moreover, UTX associates with mixed-lineage leukemia (MLL) 2/3 complexes, and during retinoic acid signaling events, the recruitment of the UTX complex to HOX genes results in H3K27 demethylation and a concomitant methylation of H3K4. Our results suggest a concerted mechanism for transcriptional activation in which cycles of H3K4 methylation by MLL2/3 are linked with the demethylation of H3K27 through UTX.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Min Gyu -- Villa, Raffaella -- Trojer, Patrick -- Norman, Jessica -- Yan, Kai-Ping -- Reinberg, Danny -- Di Croce, Luciano -- Shiekhattar, Ramin -- R01CA090758/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2007 Oct 19;318(5849):447-50. Epub 2007 Aug 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wistar Institute, 3601 Spruce Street, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17761849" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Differentiation ; Cell Line ; Cell Line, Tumor ; DNA-Binding Proteins/metabolism ; Embryonic Stem Cells ; *Genes, Homeobox ; Histone Demethylases ; Histones/*metabolism ; Humans ; Lysine/*metabolism ; Methylation ; Multigene Family ; Neoplasm Proteins/metabolism ; Nuclear Proteins/genetics/*metabolism ; Polycomb-Group Proteins ; Promoter Regions, Genetic ; Protein Processing, Post-Translational ; Recombinant Proteins/metabolism ; Repressor Proteins/*metabolism ; Signal Transduction ; Transcription, Genetic ; Transcriptional Activation ; Tretinoin/metabolism/pharmacology ; Ubiquitin/metabolism
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    A bacterial effector acts as a plant transcription factor and induces a cell size regulator (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-10-27
    Description: Pathogenicity of many Gram-negative bacteria relies on the injection of effector proteins by type III secretion into eukaryotic cells, where they modulate host signaling pathways to the pathogen's benefit. One such effector protein injected by Xanthomonas into plants is AvrBs3, which localizes to the plant cell nucleus and causes hypertrophy of plant mesophyll cells. We show that AvrBs3 induces the expression of a master regulator of cell size, upa20, which encodes a transcription factor containing a basic helix-loop-helix domain. AvrBs3 binds to a conserved element in the upa20 promoter via its central repeat region and induces gene expression through its activation domain. Thus, AvrBs3 and likely other members of this family provoke developmental reprogramming of host cells by mimicking eukaryotic transcription factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kay, Sabine -- Hahn, Simone -- Marois, Eric -- Hause, Gerd -- Bonas, Ulla -- New York, N.Y. -- Science. 2007 Oct 26;318(5850):648-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Biology, Department of Genetics, Martin-Luther-University Halle-Wittenberg, Weinbergweg 10, D-06120 Halle (Saale), Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17962565" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Bacterial Proteins/chemistry/genetics/*physiology ; Basic Helix-Loop-Helix Transcription Factors/chemistry/genetics/*physiology ; Capsicum/cytology/*genetics/*microbiology ; Cell Enlargement ; Cell Size ; Chromatin Immunoprecipitation ; Gene Expression Regulation, Plant ; Gene Silencing ; Molecular Sequence Data ; Plant Leaves/cytology/genetics/metabolism ; Plant Proteins/chemistry/genetics/metabolism/*physiology ; Promoter Regions, Genetic ; Tobacco/genetics ; Transcription, Genetic ; Xanthomonas campestris/genetics/*metabolism/pathogenicity
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    The after-hours mutant reveals a role for Fbxl3 in determining mammalian circadian period (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-04-28
    Description: By screening N-ethyl-N-nitrosourea-mutagenized animals for alterations in rhythms of wheel-running activity, we identified a mouse mutation, after hours (Afh). The mutation, a Cys(358)Ser substitution in Fbxl3, an F-box protein with leucine-rich repeats, results in long free-running rhythms of about 27 hours in homozygotes. Circadian transcriptional and translational oscillations are attenuated in Afh mice. The Afh allele significantly affected Per2 expression and delayed the rate of Cry protein degradation in Per2::Luciferase tissue slices. Our in vivo and in vitro studies reveal a central role for Fbxl3 in mammalian circadian timekeeping.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Godinho, Sofia I H -- Maywood, Elizabeth S -- Shaw, Linda -- Tucci, Valter -- Barnard, Alun R -- Busino, Luca -- Pagano, Michele -- Kendall, Rachel -- Quwailid, Mohamed M -- Romero, M Rosario -- O'neill, John -- Chesham, Johanna E -- Brooker, Debra -- Lalanne, Zuzanna -- Hastings, Michael H -- Nolan, Patrick M -- MC_U105170643/Medical Research Council/United Kingdom -- MC_U142684172/Medical Research Council/United Kingdom -- MC_U142684173/Medical Research Council/United Kingdom -- MC_U142684175/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2007 May 11;316(5826):897-900. Epub 2007 Apr 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council (MRC) Mammalian Genetics Unit, Harwell, Oxfordshire OX11 0RD, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17463252" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors ; Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics/metabolism ; CLOCK Proteins ; COS Cells ; Cell Cycle Proteins/genetics/metabolism ; Cercopithecus aethiops ; *Circadian Rhythm/genetics ; Crosses, Genetic ; Cryptochromes ; F-Box Proteins/*genetics/*physiology ; Female ; Flavoproteins/genetics/metabolism ; Gene Expression Regulation ; Liver/metabolism ; Lung/metabolism ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Molecular Sequence Data ; Nuclear Proteins/genetics/metabolism ; Period Circadian Proteins ; *Point Mutation ; Suprachiasmatic Nucleus/metabolism ; Trans-Activators/genetics/metabolism ; Transcription Factors/genetics/metabolism ; Transcription, Genetic
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    Neuronal competition and selection during memory formation (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-04-21
    Description: Competition between neurons is necessary for refining neural circuits during development and may be important for selecting the neurons that participate in encoding memories in the adult brain. To examine neuronal competition during memory formation, we conducted experiments with mice in which we manipulated the function of CREB (adenosine 3',5'-monophosphate response element-binding protein) in subsets of neurons. Changes in CREB function influenced the probability that individual lateral amygdala neurons were recruited into a fear memory trace. Our results suggest a competitive model underlying memory formation, in which eligible neurons are selected to participate in amemorytrace as a function of their relative CREB activity at the time of learning.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Han, Jin-Hee -- Kushner, Steven A -- Yiu, Adelaide P -- Cole, Christy J -- Matynia, Anna -- Brown, Robert A -- Neve, Rachael L -- Guzowski, John F -- Silva, Alcino J -- Josselyn, Sheena A -- AG13622/AG/NIA NIH HHS/ -- P01HD33098/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2007 Apr 20;316(5823):457-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Neurosciences and Mental Health, Hospital for Sick Children, 555 University Avenue, Toronto, Ontario M5G 1X8, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17446403" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/*physiology ; Animals ; Conditioning (Psychology) ; Cyclic AMP Response Element-Binding Protein/genetics/*metabolism ; Cytoskeletal Proteins/genetics/metabolism ; Fear ; Genetic Vectors ; Memory/*physiology ; Mice ; Nerve Tissue Proteins/genetics/metabolism ; Neuronal Plasticity ; Neurons/metabolism/*physiology ; Transcription, Genetic
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    Multiple functions of the IKK-related kinase IKKepsilon in interferon-mediated antiviral immunity (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-03-03
    Description: IKKepsilon is an IKK (inhibitor of nuclear factor kappaBkinase)-related kinase implicated in virus induction of interferon-beta (IFNbeta). We report that, although mice lacking IKKepsilon produce normal amounts of IFNbeta, they are hypersusceptible to viral infection because of a defect in the IFN signaling pathway. Specifically, a subset of type I IFN-stimulated genes are not activated in the absence of IKKepsilon because the interferon-stimulated gene factor 3 complex (ISGF3) does not bind to promoter elements of the affected genes. We demonstrate that IKKepsilon is activated by IFNbeta and that IKKepsilon directly phosphorylates signal transducer and activator of transcription 1 (STAT1), a component of ISGF3. We conclude that IKKepsilon plays a critical role in the IFN-inducible antiviral transcriptional response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tenoever, Benjamin R -- Ng, Sze-Ling -- Chua, Mark A -- McWhirter, Sarah M -- Garcia-Sastre, Adolfo -- Maniatis, Tom -- F31 AI056678/AI/NIAID NIH HHS/ -- P01AI058113/AI/NIAID NIH HHS/ -- R01AI46954/AI/NIAID NIH HHS/ -- U19AI62623/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2007 Mar 2;315(5816):1274-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Harvard University, 7 Divinity Avenue, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17332413" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Deaminase/genetics/metabolism ; Animals ; Cells, Cultured ; Dimerization ; *Gene Expression Regulation ; I-kappa B Kinase/genetics/*metabolism ; *Influenza A Virus, H1N1 Subtype/immunology/physiology ; Interferon-Stimulated Gene Factor 3/metabolism ; Interferon-beta/*immunology/metabolism ; Lung/pathology/virology ; Mice ; Mice, Knockout ; Orthomyxoviridae Infections/*immunology/metabolism/pathology/virology ; Phosphorylation ; Promoter Regions, Genetic ; RNA-Binding Proteins ; STAT1 Transcription Factor/metabolism ; STAT2 Transcription Factor/metabolism ; Signal Transduction ; Transcription, Genetic ; Viral Load ; Virus Replication
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    Hd3a protein is a mobile flowering signal in rice (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-04-21
    Description: Florigen, the mobile signal that moves from an induced leaf to the shoot apex and causes flowering, has eluded identification since it was first proposed 70 years ago. Understanding the nature of the mobile flowering signal would provide a key insight into the molecular mechanism of floral induction. Recent studies suggest that the Arabidopsis FLOWERING LOCUS T (FT) gene is a candidate for encoding florigen. We show that the protein encoded by Hd3a, a rice ortholog of FT, moves from the leaf to the shoot apical meristem and induces flowering in rice. These results suggest that the Hd3a protein may be the rice florigen.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tamaki, Shojiro -- Matsuo, Shoichi -- Wong, Hann Ling -- Yokoi, Shuji -- Shimamoto, Ko -- New York, N.Y. -- Science. 2007 May 18;316(5827):1033-6. Epub 2007 Apr 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Plant Molecular Genetics, Nara Institute of Science and Technology, 8916-5 Takayama, Ikoma 630-0101, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17446351" target="_blank"〉PubMed〈/a〉
    Keywords: Flowers/*growth & development ; Gene Expression Regulation, Plant ; Light ; Meristem/metabolism ; Oryza/genetics/growth & development/*physiology ; Periodicity ; Plant Leaves/genetics/metabolism ; Plant Proteins/genetics/*metabolism ; Plant Shoots/genetics/metabolism ; Plant Stems/metabolism ; Plants, Genetically Modified ; Protein Transport ; RNA, Messenger/genetics/metabolism ; RNA, Plant/genetics/metabolism ; Recombinant Fusion Proteins/metabolism ; *Signal Transduction ; Transcription, Genetic
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    The maternal-zygotic transition: death and birth of RNAs (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-04-21
    Description: Maternal gene products drive early development when the newly formed embryo is transcriptionally inactive. During the maternal-zygotic transition, embryonic transcription is initiated and many maternal RNAs are degraded. Multiple mechanisms regulate the birth of zygotic RNAs and the death of maternal RNAs. Genome activation appears to rely in part on the sequestration of transcriptional repressors by the exponentially increasing amount of DNA during cleavage divisions. Maternal RNA degradation is induced by the binding of proteins and microRNAs to the 3' untranslated region of target RNAs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schier, Alexander F -- New York, N.Y. -- Science. 2007 Apr 20;316(5823):406-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Harvard Stem Cell Institute, Center for Brain Science, Broad Institute, Harvard University, 16 Divinity Avenue, Room 1027, Cambridge, MA 02138, USA. schier@fas.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17446392" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions ; Animals ; Cell Cycle ; Embryonic Development ; Female ; *Gene Expression Regulation, Developmental ; Gene Silencing ; MicroRNAs ; *RNA Stability ; RNA, Messenger/*metabolism ; RNA, Messenger, Stored/*metabolism ; RNA-Binding Proteins/metabolism ; Transcription, Genetic ; Zygote/cytology/*metabolism
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    A MicroRNA feedback circuit in midbrain dopamine neurons (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-09-01
    Description: MicroRNAs (miRNAs) are evolutionarily conserved, 18- to 25-nucleotide, non-protein coding transcripts that posttranscriptionally regulate gene expression during development. miRNAs also occur in postmitotic cells, such as neurons in the mammalian central nervous system, but their function is less well characterized. We investigated the role of miRNAs in mammalian midbrain dopaminergic neurons (DNs). We identified a miRNA, miR-133b, that is specifically expressed in midbrain DNs and is deficient in midbrain tissue from patients with Parkinson's disease. miR-133b regulates the maturation and function of midbrain DNs within a negative feedback circuit that includes the paired-like homeodomain transcription factor Pitx3. We propose a role for this feedback circuit in the fine-tuning of dopaminergic behaviors such as locomotion.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2782470/" 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/PMC2782470/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Jongpil -- Inoue, Keiichi -- Ishii, Jennifer -- Vanti, William B -- Voronov, Sergey V -- Murchison, Elizabeth -- Hannon, Gregory -- Abeliovich, Asa -- R01 NS064433/NS/NINDS NIH HHS/ -- R01 NS064433-01/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2007 Aug 31;317(5842):1220-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Pathology and Neurology, Center for Neurobiology and Behavior, and Taub Institute, Columbia University, College of Physicians and Surgeons 15-403, 630 West 168th Street, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17761882" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions/metabolism ; Aged ; Aged, 80 and over ; Animals ; Cell Differentiation ; Cell Line ; Cells, Cultured ; Dopamine/*metabolism ; Embryonic Stem Cells ; *Feedback, Physiological ; Female ; Gene Expression Regulation ; Homeodomain Proteins/*metabolism ; Humans ; Locomotion ; Male ; Mesencephalon/cytology/*metabolism ; Mice ; MicroRNAs/*metabolism ; Middle Aged ; Models, Biological ; Neurons/cytology/*metabolism ; Parkinson Disease/metabolism ; Rats ; Ribonuclease III/genetics/metabolism ; Transcription Factors/*metabolism ; Transcription, Genetic
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    Negative regulation of toll-like receptor signaling by NF-kappaB p50 ubiquitination blockade (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-08-04
    Description: Toll-like receptors (TLRs) trigger the production of inflammatory cytokines and shape adaptive and innate immunity to pathogens. We report the identification of B cell leukemia (Bcl)-3 as an essential negative regulator of TLR signaling. By blocking ubiquitination of p50, a member of the nuclear factor (NF)-kappaB family, Bcl-3 stabilizes a p50 complex that inhibits gene transcription. As a consequence, Bcl-3-deficient mice and cells were found to be hypersensitive to TLR activation and unable to control responses to lipopolysaccharides. Thus, p50 ubiquitination blockade by Bcl-3 limits the strength of TLR responses and maintains innate immune homeostasis. These findings indicate that the p50 ubiquitination pathway can be selectively targeted to control deleterious inflammatory diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carmody, Ruaidhri J -- Ruan, Qingguo -- Palmer, Scott -- Hilliard, Brendan -- Chen, Youhai H -- AI069289/AI/NIAID NIH HHS/ -- AI50059/AI/NIAID NIH HHS/ -- DK070691/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2007 Aug 3;317(5838):675-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17673665" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cells, Cultured ; DNA/metabolism ; Female ; Half-Life ; Immune Tolerance ; Immunity, Innate ; Lipopolysaccharides/immunology ; Macrophage Activation ; Macrophages, Peritoneal/*immunology/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; NF-kappa B p50 Subunit/*metabolism ; Promoter Regions, Genetic ; Proto-Oncogene Proteins/genetics/*metabolism ; *Signal Transduction ; Toll-Like Receptors/*metabolism ; Transcription Factor RelA/metabolism ; Transcription Factors/genetics/*metabolism ; Transcription, Genetic ; Tumor Necrosis Factor-alpha/genetics/metabolism ; Ubiquitin/metabolism
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    Effects of aneuploidy on cellular physiology and cell division in haploid yeast (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-08-19
    Description: Aneuploidy is a condition frequently found in tumor cells, but its effect on cellular physiology is not known. We have characterized one aspect of aneuploidy: the gain of extra chromosomes. We created a collection of haploid yeast strains that each bear an extra copy of one or more of almost all of the yeast chromosomes. Their characterization revealed that aneuploid strains share a number of phenotypes, including defects in cell cycle progression, increased glucose uptake, and increased sensitivity to conditions interfering with protein synthesis and protein folding. These phenotypes were observed only in strains carrying additional yeast genes, which indicates that they reflect the consequences of additional protein production as well as the resulting imbalances in cellular protein composition. We conclude that aneuploidy causes not only a proliferative disadvantage but also a set of phenotypes that is independent of the identity of the individual extra chromosomes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Torres, Eduardo M -- Sokolsky, Tanya -- Tucker, Cheryl M -- Chan, Leon Y -- Boselli, Monica -- Dunham, Maitreya J -- Amon, Angelika -- GM071508/GM/NIGMS NIH HHS/ -- GM56800/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2007 Aug 17;317(5840):916-24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Cancer Research, Howard Hughes Medical Institute, Massachusetts Institute of Technology, E17-233, 40 Ames Street, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17702937" target="_blank"〉PubMed〈/a〉
    Keywords: *Aneuploidy ; Cell Division ; *Cell Proliferation ; Chromosomes, Fungal/genetics ; G1 Phase ; Gene Expression Regulation, Fungal ; Genes, Fungal ; Glucose/metabolism ; Haploidy ; Phenotype ; Protein Synthesis Inhibitors/pharmacology ; Saccharomyces cerevisiae/cytology/*genetics/*physiology ; Saccharomyces cerevisiae Proteins/biosynthesis/metabolism ; Temperature ; Transcription, Genetic
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    Life with oxygen (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-10-06
    Description: The survival of all metazoan organisms is dependent on the regulation of O2 delivery and utilization to maintain a balance between the generation of energy and production of potentially toxic oxidants. Hypoxia-inducible factor 1 (HIF-1) is a transcription factor that functions as a master regulator of oxygen homeostasis and has essential roles in metazoan development, physiology, and disease pathogenesis. Remarkable progress has been made in delineating the molecular mechanisms whereby changes in cellular oxygenation are transduced to the nucleus as changes in gene transcription through the activity of HIF-1. Pharmacologic agents that activate or inhibit the hypoxia signal transduction pathway may be useful therapies for ischemic and neoplastic disorders, respectively, which are the major causes of mortality in industrialized societies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Semenza, Gregg L -- New York, N.Y. -- Science. 2007 Oct 5;318(5847):62-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, Johns Hopkins University School of Medicine, Broadway Research Building, Suite 671, 733 North Broadway, Baltimore, MD 21205, USA. gsemenza@jhmi.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17916722" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; Cell Hypoxia/physiology ; Energy Metabolism ; Gene Expression Regulation ; Homeostasis ; Humans ; Hypoxia-Inducible Factor 1/chemistry/*metabolism ; Ischemia/metabolism/therapy ; Neoplasms/metabolism/pathology/therapy ; Oxygen/*metabolism ; *Signal Transduction ; Transcription, Genetic
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    Telomeric repeat containing RNA and RNA surveillance factors at mammalian chromosome ends (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-10-06
    Description: Telomeres, the DNA-protein complexes located at the end of linear eukaryotic chromosomes, are essential for chromosome stability. Until now, telomeres have been considered to be transcriptionally silent. We demonstrate that mammalian telomeres are transcribed into telomeric repeat-containing RNA (TERRA). TERRA molecules are heterogeneous in length, are transcribed from several subtelomeric loci toward chromosome ends, and localize to telomeres. We also show that suppressors with morphogenetic defects in genitalia (SMG) proteins, which are effectors of nonsense-mediated messenger RNA decay, are enriched at telomeres in vivo, negatively regulate TERRA association with chromatin, and protect chromosome ends from telomere loss. Thus, telomeres are actively transcribed into TERRA, and SMG factors represent a molecular link between TERRA regulation and the maintenance of telomere integrity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Azzalin, Claus M -- Reichenbach, Patrick -- Khoriauli, Lela -- Giulotto, Elena -- Lingner, Joachim -- New York, N.Y. -- Science. 2007 Nov 2;318(5851):798-801. Epub 2007 Oct 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Swiss Institute for Experimental Cancer Research (ISREC), CH-1066 Epalinges, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17916692" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Blotting, Northern ; Cells, Cultured ; Chromosomes, Human ; Chromosomes, Mammalian ; HeLa Cells ; Humans ; In Situ Hybridization, Fluorescence ; Mice ; Molecular Sequence Data ; Proteins/metabolism ; RNA/*genetics ; Repetitive Sequences, Nucleic Acid ; Telomerase/physiology ; Telomere/*genetics ; Transcription, Genetic ; Tumor Cells, Cultured
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    A hexanucleotide element directs microRNA nuclear import (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-01-06
    Description: MicroRNAs (miRNAs) negatively regulate partially complementary target messenger RNAs. Target selection in animals is dictated primarily by sequences at the miRNA 5' end. We demonstrated that despite their small size, specific miRNAs contain additional sequence elements that control their posttranscriptional behavior, including their subcellular localization. We showed that human miR-29b, in contrast to other studied animal miRNAs, is predominantly localized to the nucleus. The distinctive hexanucleotide terminal motif of miR-29b acts as a transferable nuclear localization element that directs nuclear enrichment of miRNAs or small interfering RNAs to which it is attached. Our results indicate that miRNAs sharing common 5' sequences, considered to be largely redundant, might have distinct functions because of the influence of cis-acting regulatory motifs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hwang, Hun-Way -- Wentzel, Erik A -- Mendell, Joshua T -- New York, N.Y. -- Science. 2007 Jan 5;315(5808):97-100.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Human Genetics and Molecular Biology, McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17204650" target="_blank"〉PubMed〈/a〉
    Keywords: Active Transport, Cell Nucleus ; Animals ; Apoptosis ; Base Sequence ; Cell Nucleus/*metabolism ; HeLa Cells ; Humans ; Mice ; MicroRNAs/*chemistry/*metabolism ; Mitosis ; Mutation ; NIH 3T3 Cells ; Oligoribonucleotides/chemistry/*metabolism ; RNA Processing, Post-Transcriptional ; RNA Stability ; RNA, Small Interfering ; Reverse Transcriptase Polymerase Chain Reaction ; Ribonuclease III/metabolism ; Transcription, Genetic
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    Genomics. DNA study forces rethink of what it means to be a gene (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-06-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, Elizabeth -- New York, N.Y. -- Science. 2007 Jun 15;316(5831):1556-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17569836" target="_blank"〉PubMed〈/a〉
    Keywords: DNA/*genetics ; Exons ; *Genes ; Genetic Code ; *Genome, Human ; *Genomics ; Humans ; Promoter Regions, Genetic ; RNA/genetics ; RNA, Messenger/genetics ; RNA, Untranslated/genetics ; Transcription Initiation Site ; Transcription, Genetic
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  • 86
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    Epigenetic flexibility underlying lineage choices in the adaptive immune system (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-08-04
    Description: Although fundamental models have emerged in recent years describing how chromatin and transcription regulation interface with one another in the developing immune system, the order of events and their biological impact are still being resolved. Recent advances have provided a flexible, rather than static, view of chromatin regulation to reveal how both positive and negative forces work concomitantly to establish specific chromatin structures and regulate gene expression. The challenge will now be to explore new epigenetic models and validate them during lymphocyte development, with the ultimate goal of unraveling the long-sought mechanisms that support the emerging complexity of the adaptive immune response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kioussis, Dimitris -- Georgopoulos, Katia -- MC_U117512796/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2007 Aug 3;317(5838):620-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Immunology, Medical Research Council (MRC) National Institute for Medical Research, The Ridgeway, London NW7 1AA, UK. dkiouss@nimr.mrc.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17673651" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Lineage ; Cell Nucleus/metabolism ; Chromatin/*metabolism ; *Epigenesis, Genetic ; *Gene Expression Regulation ; Gene Silencing ; Hematopoietic Stem Cells/cytology/metabolism ; Humans ; Lymphocytes/cytology/*metabolism ; *Lymphopoiesis ; Transcription, Genetic
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  • 87
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    Molecular biology. Unlocking cell fate (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-10-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rivenbark, Ashley G -- Strahl, Brian D -- New York, N.Y. -- Science. 2007 Oct 19;318(5849):403-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, UNC Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17947570" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; *Cell Lineage ; Chromatin/metabolism ; Embryonic Development ; *Epigenesis, Genetic ; Gene Expression Regulation, Developmental ; Genes, Homeobox ; Histone Code ; Histones/*metabolism ; Humans ; Jumonji Domain-Containing Histone Demethylases ; Methylation ; Promoter Regions, Genetic ; *Protein Processing, Post-Translational ; Receptors, Cell Surface/metabolism ; Transcription, Genetic
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  • 88
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    An evolutionarily conserved mechanism delimiting SHR movement defines a single layer of endodermis in plants (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-04-21
    Description: Intercellular protein movement plays a critical role in animal and plant development. SHORTROOT (SHR) is a moving transcription factor essential for endodermis specification in the Arabidopsis root. Unlike diffusible animal morphogens, which form a gradient across multiple cell layers, SHR movement is limited to essentially one cell layer. However, the molecular mechanism is unknown. We show that SCARECROW (SCR) blocks SHR movement by sequestering it into the nucleus through protein-protein interaction and a safeguard mechanism that relies on a SHR/SCR-dependent positive feedback loop for SCR transcription. Our studies with SHR and SCR homologs from rice suggest that this mechanism is evolutionarily conserved, providing a plausible explanation why nearly all plants have a single layer of endodermis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cui, Hongchang -- Levesque, Mitchell P -- Vernoux, Teva -- Jung, Jee W -- Paquette, Alice J -- Gallagher, Kimberly L -- Wang, Jean Y -- Blilou, Ikram -- Scheres, Ben -- Benfey, Philip N -- R01-GM043778/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2007 Apr 20;316(5823):421-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology and Institute for Genome Sciences and Policy, Duke University, Durham, NC 27708, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17446396" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/cytology/genetics/growth & development/*metabolism ; Arabidopsis Proteins/genetics/*metabolism ; Biological Evolution ; Cell Nucleus/metabolism ; Feedback, Physiological ; Gene Expression ; Genes, Plant ; Models, Biological ; Oligonucleotide Array Sequence Analysis ; Oryza/genetics/metabolism ; Plant Proteins/genetics/metabolism ; Plant Roots/*cytology/genetics/growth & development/*metabolism ; Plants, Genetically Modified ; Promoter Regions, Genetic ; Protein Binding ; Protein Transport ; Recombinant Fusion Proteins/metabolism ; Transcription Factors/genetics/*metabolism ; Transcription, Genetic
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  • 89
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    Genomic minimalism in the early diverging intestinal parasite Giardia lamblia (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-09-29
    Description: The genome of the eukaryotic protist Giardia lamblia, an important human intestinal parasite, is compact in structure and content, contains few introns or mitochondrial relics, and has simplified machinery for DNA replication, transcription, RNA processing, and most metabolic pathways. Protein kinases comprise the single largest protein class and reflect Giardia's requirement for a complex signal transduction network for coordinating differentiation. Lateral gene transfer from bacterial and archaeal donors has shaped Giardia's genome, and previously unknown gene families, for example, cysteine-rich structural proteins, have been discovered. Unexpectedly, the genome shows little evidence of heterozygosity, supporting recent speculations that this organism is sexual. This genome sequence will not only be valuable for investigating the evolution of eukaryotes, but will also be applied to the search for new therapeutics for this parasite.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morrison, Hilary G -- McArthur, Andrew G -- Gillin, Frances D -- Aley, Stephen B -- Adam, Rodney D -- Olsen, Gary J -- Best, Aaron A -- Cande, W Zacheus -- Chen, Feng -- Cipriano, Michael J -- Davids, Barbara J -- Dawson, Scott C -- Elmendorf, Heidi G -- Hehl, Adrian B -- Holder, Michael E -- Huse, Susan M -- Kim, Ulandt U -- Lasek-Nesselquist, Erica -- Manning, Gerard -- Nigam, Anuranjini -- Nixon, Julie E J -- Palm, Daniel -- Passamaneck, Nora E -- Prabhu, Anjali -- Reich, Claudia I -- Reiner, David S -- Samuelson, John -- Svard, Staffan G -- Sogin, Mitchell L -- AI42488/AI/NIAID NIH HHS/ -- AI43273/AI/NIAID NIH HHS/ -- AI51687/AI/NIAID NIH HHS/ -- R01 AI043273/AI/NIAID NIH HHS/ -- R01 AI048082/AI/NIAID NIH HHS/ -- R01 HG004164/HG/NHGRI NIH HHS/ -- R01 HG004164-01/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2007 Sep 28;317(5846):1921-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Marine Biological Laboratory, Woods Hole, MA 02543-1015, USA. morrison@mbl.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17901334" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Biological Evolution ; DNA Replication/genetics ; *Eukaryotic Cells ; Gene Transfer, Horizontal ; Genes, Protozoan ; *Genome, Protozoan ; Genomics ; Giardia lamblia/classification/*genetics/physiology ; Metabolic Networks and Pathways/genetics ; Molecular Sequence Data ; Phylogeny ; Protein Kinases/genetics/metabolism ; Protozoan Proteins/chemistry/genetics/metabolism ; RNA Processing, Post-Transcriptional ; Signal Transduction ; Transcription, Genetic
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  • 90
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    Proteasome-independent functions of ubiquitin in endocytosis and signaling (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-01-16
    Description: Ubiquitination is a reversible posttranslational modification of cellular proteins, in which a 76-amino acid polypeptide, ubiquitin, is primarily attached to the epsilon-amino group of lysines in target proteins. Ubiquitination is a major player in regulating a broad host of cellular processes, including cell division, differentiation, signal transduction, protein trafficking, and quality control. Aberrations in the ubiquitination system are implicated in pathogenesis of some diseases, certain malignancies, neurodegenerative disorders, and pathologies of the inflammatory immune response. Here, we discuss the proteasome-independent roles of ubiquitination in signaling and endocytosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mukhopadhyay, Debdyuti -- Riezman, Howard -- New York, N.Y. -- Science. 2007 Jan 12;315(5809):201-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Geneva, 30 Quai Ernest Ansermet, CH-1211 Geneva, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17218518" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA Replication ; Disease ; *Endocytosis ; Endosomes/metabolism ; Humans ; Models, Biological ; Neoplasms/metabolism ; Neurodegenerative Diseases/metabolism ; Proteasome Endopeptidase Complex/metabolism ; Protein Sorting Signals ; Protein Transport ; Proteins/*metabolism ; *Signal Transduction ; Transcription, Genetic ; Ubiquitin/*metabolism
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  • 91
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    Combined action of PHD and chromo domains directs the Rpd3S HDAC to transcribed chromatin (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-05-19
    Description: Nucleosomes must be deacetylated behind elongating RNA polymerase II to prevent cryptic initiation of transcription within the coding region. RNA polymerase II signals for deacetylation through the methylation of histone H3 lysine 36 (H3K36), which provides the recruitment signal for the Rpd3S histone deacetylase complex (HDAC). The recognition of methyl H3K36 by Rpd3S requires the chromodomain of its Eaf3 subunit. Paradoxically, Eaf3 is also a subunit of the NuA4 acetyltransferase complex, yet NuA4 does not recognize methyl H3K36 nucleosomes. In Saccharomyces cerevisiae, we found that methyl H3K36 nucleosome recognition by Rpd3S also requires the plant homeobox domain (PHD) of its Rco1 subunit. Thus, the coupled chromo and PHD domains of Rpd3S specify recognition of the methyl H3K36 mark, demonstrating the first combinatorial domain requirement within a protein complex to read a specific histone code.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Bing -- Gogol, Madelaine -- Carey, Mike -- Lee, Daeyoup -- Seidel, Chris -- Workman, Jerry L -- New York, N.Y. -- Science. 2007 May 18;316(5827):1050-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stowers Institute for Medical Research, 1000 East 50th Street, Kansas City, MO 64110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17510366" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Acetyltransferases/chemistry/metabolism ; Chromatin/*metabolism ; Chromatin Immunoprecipitation ; DNA, Fungal/metabolism ; Histone Acetyltransferases/chemistry/metabolism ; Histone Code ; Histone Deacetylases/*chemistry/*metabolism ; Histones/*metabolism ; Methylation ; Mutation ; Nucleosomes/*metabolism ; Oligonucleotide Array Sequence Analysis ; Open Reading Frames ; Protein Structure, Tertiary ; Protein Subunits/chemistry/metabolism ; Saccharomyces cerevisiae/genetics/*metabolism ; Saccharomyces cerevisiae Proteins/chemistry/genetics/*metabolism ; Transcription, Genetic
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  • 92
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    Germ versus soma decisions: lessons from flies and worms (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-04-21
    Description: The early embryo is formed by the fusion of two germ cells that must generate not only all of the nonreproductive somatic cell types of its body but also the germ cells for the next generation. Therefore, embryo cells face a crucial decision: whether to develop as germ or soma. How is this fundamental decision made and germ cell fate maintained during development? Studies in the nematode worm Caenorhabditis elegans and fruit fly Drosophila identify some of the decision-making strategies, including segregation of a specialized germ plasm and global transcriptional regulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Strome, Susan -- Lehmann, Ruth -- New York, N.Y. -- Science. 2007 Apr 20;316(5823):392-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Indiana University, Bloomington, IN 47405, USA. sstrome@indiana.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17446385" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/*embryology/genetics ; Caenorhabditis elegans Proteins/metabolism ; Cell Differentiation ; Cell Division ; Cell Lineage ; Drosophila/*embryology/genetics ; Drosophila Proteins/metabolism ; Embryo, Nonmammalian/*cytology/physiology ; Embryonic Development ; Gene Expression Regulation, Developmental ; Germ Cells/*cytology/physiology ; Organelles/physiology ; Transcription, Genetic
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    Patched1 regulates hedgehog signaling at the primary cilium (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-07-21
    Description: Primary cilia are essential for transduction of the Hedgehog (Hh) signal in mammals. We investigated the role of primary cilia in regulation of Patched1 (Ptc1), the receptor for Sonic Hedgehog (Shh). Ptc1 localized to cilia and inhibited Smoothened (Smo) by preventing its accumulation within cilia. When Shh bound to Ptc1, Ptc1 left the cilia, leading to accumulation of Smo and activation of signaling. Thus, primary cilia sense Shh and transduce signals that play critical roles in development, carcinogenesis, and stem cell function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rohatgi, Rajat -- Milenkovic, Ljiljana -- Scott, Matthew P -- R01 CA088060/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2007 Jul 20;317(5836):372-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Developmental Biology, Genetics, and Bioengineering and Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17641202" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Membrane/metabolism ; Cells, Cultured ; Cilia/*metabolism ; Cyclohexylamines/pharmacology ; Embryo, Mammalian/metabolism ; Hedgehog Proteins/agonists/*metabolism ; Hydroxycholesterols/pharmacology ; Mesoderm/metabolism ; Mice ; NIH 3T3 Cells ; Protein Binding ; Receptors, Cell Surface/genetics/*metabolism ; Receptors, G-Protein-Coupled/metabolism ; *Signal Transduction ; Thiophenes/pharmacology ; Transcription, Genetic ; Transfection
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    Plant pathogen recognition mediated by promoter activation of the pepper Bs3 resistance gene (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-10-27
    Description: Plant disease resistance (R) proteins recognize matching pathogen avirulence proteins. Alleles of the pepper R gene Bs3 mediate recognition of the Xanthomonas campestris pv. vesicatoria (Xcv) type III effector protein AvrBs3 and its deletion derivative AvrBs3Deltarep16. Pepper Bs3 and its allelic variant Bs3-E encode flavin monooxygenases with a previously unknown structure and are transcriptionally activated by the Xcv effector proteins AvrBs3 and AvrBs3Deltarep16, respectively. We found that recognition specificity resides in the Bs3 and Bs3-E promoters and is determined by binding of AvrBs3 or AvrBs3Deltarep16 to a defined promoter region. Our data suggest a recognition mechanism in which the Avr protein binds and activates the promoter of the cognate R gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Romer, Patrick -- Hahn, Simone -- Jordan, Tina -- Strauss, Tina -- Bonas, Ulla -- Lahaye, Thomas -- New York, N.Y. -- Science. 2007 Oct 26;318(5850):645-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Biology, Department of Genetics, Martin-Luther-University Halle-Wittenberg, D-06099 Halle (Saale), Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17962564" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Bacterial Proteins/genetics/*metabolism ; Base Sequence ; Capsicum/*genetics/*microbiology ; Chromosomes, Artificial, Bacterial ; Gene Expression Regulation, Plant ; *Genes, Plant ; Mixed Function Oxygenases/chemistry/*genetics ; Molecular Sequence Data ; Plant Diseases/immunology/microbiology ; Plant Leaves/genetics/metabolism ; Plant Proteins/chemistry/genetics ; *Promoter Regions, Genetic ; Tobacco/genetics ; Transcription, Genetic ; Transformation, Genetic ; Xanthomonas campestris/genetics/metabolism/*pathogenicity
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    Boron-toxicity tolerance in barley arising from efflux transporter amplification (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-12-01
    Description: Both limiting and toxic soil concentrations of the essential micronutrient boron represent major limitations to crop production worldwide. We identified Bot1, a BOR1 ortholog, as the gene responsible for the superior boron-toxicity tolerance of the Algerian barley landrace Sahara 3771 (Sahara). Bot1 was located at the tolerance locus by high-resolution mapping. Compared to intolerant genotypes, Sahara contains about four times as many Bot1 gene copies, produces substantially more Bot1 transcript, and encodes a Bot1 protein with a higher capacity to provide tolerance in yeast. Bot1 transcript levels identified in barley tissues are consistent with a role in limiting the net entry of boron into the root and in the disposal of boron from leaves via hydathode guttation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sutton, Tim -- Baumann, Ute -- Hayes, Julie -- Collins, Nicholas C -- Shi, Bu-Jun -- Schnurbusch, Thorsten -- Hay, Alison -- Mayo, Gwenda -- Pallotta, Margaret -- Tester, Mark -- Langridge, Peter -- New York, N.Y. -- Science. 2007 Nov 30;318(5855):1446-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Australian Centre for Plant Functional Genomics, School of Agriculture, Food and Wine, University of Adelaide, Waite Campus, Private Mail Bag 1, Glen Osmond, South Australia 5064, Australia. tim.sutton@acpfg.com.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18048688" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Biological Transport ; Boron/metabolism/*toxicity ; Boron Compounds/*metabolism/*toxicity ; Chromosome Mapping ; *Genes, Plant ; Hordeum/*drug effects/*genetics/metabolism ; Membrane Transport Proteins/chemistry/*genetics/metabolism ; Molecular Sequence Data ; Plant Lectins/genetics/metabolism ; Plant Proteins/chemistry/genetics/metabolism ; Plant Roots/genetics/metabolism ; Quantitative Trait Loci ; Saccharomyces cerevisiae/genetics/growth & development/metabolism ; Transcription, Genetic
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  • 96
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    Functional architecture and evolution of transcriptional elements that drive gene coexpression (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-09-18
    Description: Transcriptional coexpression of interacting gene products is required for complex molecular processes; however, the function and evolution of cis-regulatory elements that orchestrate coexpression remain largely unexplored. We mutagenized 19 regulatory elements that drive coexpression of Ciona muscle genes and obtained quantitative estimates of the cis-regulatory activity of the 77 motifs that comprise these elements. We found that individual motif activity ranges broadly within and among elements, and among different instantiations of the same motif type. The activity of orthologous motifs is strongly constrained, although motif arrangement, type, and activity vary greatly among the elements of different co-regulated genes. Thus, the syntactical rules governing this regulatory function are flexible but become highly constrained evolutionarily once they are established in a particular element.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, Christopher D -- Johnson, David S -- Sidow, Arend -- New York, N.Y. -- Science. 2007 Sep 14;317(5844):1557-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Stanford University School of Medicine, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17872446" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ciona intestinalis/embryology/*genetics ; Creatine Kinase/genetics ; Embryo, Nonmammalian/metabolism ; *Evolution, Molecular ; *Gene Expression Regulation, Developmental ; Muscle Proteins/genetics ; Muscles/cytology/embryology/metabolism ; Mutation ; *Regulatory Sequences, Nucleic Acid ; *Response Elements ; Selection, Genetic ; Transcription, Genetic ; Urochordata/embryology/*genetics
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    The Arabidopsis circadian clock incorporates a cADPR-based feedback loop (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-12-18
    Description: Transcriptional feedback loops are a feature of circadian clocks in both animals and plants. We show that the plant circadian clock also incorporates the cytosolic signaling molecule cyclic adenosine diphosphate ribose (cADPR). cADPR modulates the circadian oscillator's transcriptional feedback loops and drives circadian oscillations of Ca2+ release. The effects of antagonists of cADPR signaling, manipulation of cADPR synthesis, and mathematical simulation of the interaction of cADPR with the circadian clock indicate that cADPR forms a feedback loop within the plant circadian clock.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dodd, Antony N -- Gardner, Michael J -- Hotta, Carlos T -- Hubbard, Katharine E -- Dalchau, Neil -- Love, John -- Assie, Jean-Maurice -- Robertson, Fiona C -- Jakobsen, Mia Kyed -- Goncalves, Jorge -- Sanders, Dale -- Webb, Alex A R -- BB/E002692/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- P19207/Biotechnology and Biological Sciences Research Council/United Kingdom -- New York, N.Y. -- Science. 2007 Dec 14;318(5857):1789-92. Epub 2007 Nov 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Plant Sciences, University of Cambridge, Downing Street, Cambridge CB2 3EA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18084825" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/genetics/*metabolism ; Calcium/metabolism ; Calcium Signaling/drug effects ; *Circadian Rhythm/genetics ; Cyclic ADP-Ribose/*metabolism ; *Feedback, Physiological ; Gene Expression Profiling ; Gene Expression Regulation, Plant ; Models, Biological ; Niacinamide/pharmacology ; Plant Leaves/metabolism ; Signal Transduction ; Transcription, Genetic
    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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  • 98
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    Genome sequence of Aedes aegypti, a major arbovirus vector (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-05-19
    Description: We present a draft sequence of the genome of Aedes aegypti, the primary vector for yellow fever and dengue fever, which at approximately 1376 million base pairs is about 5 times the size of the genome of the malaria vector Anopheles gambiae. Nearly 50% of the Ae. aegypti genome consists of transposable elements. These contribute to a factor of approximately 4 to 6 increase in average gene length and in sizes of intergenic regions relative to An. gambiae and Drosophila melanogaster. Nonetheless, chromosomal synteny is generally maintained among all three insects, although conservation of orthologous gene order is higher (by a factor of approximately 2) between the mosquito species than between either of them and the fruit fly. An increase in genes encoding odorant binding, cytochrome P450, and cuticle domains relative to An. gambiae suggests that members of these protein families underpin some of the biological differences between the two mosquito species.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2868357/" 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/PMC2868357/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nene, Vishvanath -- Wortman, Jennifer R -- Lawson, Daniel -- Haas, Brian -- Kodira, Chinnappa -- Tu, Zhijian Jake -- Loftus, Brendan -- Xi, Zhiyong -- Megy, Karyn -- Grabherr, Manfred -- Ren, Quinghu -- Zdobnov, Evgeny M -- Lobo, Neil F -- Campbell, Kathryn S -- Brown, Susan E -- Bonaldo, Maria F -- Zhu, Jingsong -- Sinkins, Steven P -- Hogenkamp, David G -- Amedeo, Paolo -- Arensburger, Peter -- Atkinson, Peter W -- Bidwell, Shelby -- Biedler, Jim -- Birney, Ewan -- Bruggner, Robert V -- Costas, Javier -- Coy, Monique R -- Crabtree, Jonathan -- Crawford, Matt -- Debruyn, Becky -- Decaprio, David -- Eiglmeier, Karin -- Eisenstadt, Eric -- El-Dorry, Hamza -- Gelbart, William M -- Gomes, Suely L -- Hammond, Martin -- Hannick, Linda I -- Hogan, James R -- Holmes, Michael H -- Jaffe, David -- Johnston, J Spencer -- Kennedy, Ryan C -- Koo, Hean -- Kravitz, Saul -- Kriventseva, Evgenia V -- Kulp, David -- Labutti, Kurt -- Lee, Eduardo -- Li, Song -- Lovin, Diane D -- Mao, Chunhong -- Mauceli, Evan -- Menck, Carlos F M -- Miller, Jason R -- Montgomery, Philip -- Mori, Akio -- Nascimento, Ana L -- Naveira, Horacio F -- Nusbaum, Chad -- O'leary, Sinead -- Orvis, Joshua -- Pertea, Mihaela -- Quesneville, Hadi -- Reidenbach, Kyanne R -- Rogers, Yu-Hui -- Roth, Charles W -- Schneider, Jennifer R -- Schatz, Michael -- Shumway, Martin -- Stanke, Mario -- Stinson, Eric O -- Tubio, Jose M C -- Vanzee, Janice P -- Verjovski-Almeida, Sergio -- Werner, Doreen -- White, Owen -- Wyder, Stefan -- Zeng, Qiandong -- Zhao, Qi -- Zhao, Yongmei -- Hill, Catherine A -- Raikhel, Alexander S -- Soares, Marcelo B -- Knudson, Dennis L -- Lee, Norman H -- Galagan, James -- Salzberg, Steven L -- Paulsen, Ian T -- Dimopoulos, George -- Collins, Frank H -- Birren, Bruce -- Fraser-Liggett, Claire M -- Severson, David W -- 079059/Wellcome Trust/United Kingdom -- 5 R01 AI61576-2/AI/NIAID NIH HHS/ -- R01 AI059492/AI/NIAID NIH HHS/ -- R01 LM006845/LM/NLM NIH HHS/ -- R01 LM006845-08/LM/NLM NIH HHS/ -- R37 AI024716/AI/NIAID NIH HHS/ -- UO1 AI50936/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2007 Jun 22;316(5832):1718-23. Epub 2007 May 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Genomic Research, 9712 Medical Center Drive, Rockville, MD 20850, USA. nene@tigr.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17510324" target="_blank"〉PubMed〈/a〉
    Keywords: Aedes/*genetics/metabolism ; Animals ; Anopheles gambiae/genetics/metabolism ; Arboviruses ; Base Sequence ; DNA Transposable Elements ; Dengue/prevention & control/transmission ; Drosophila melanogaster/genetics ; Female ; Genes, Insect ; *Genome, Insect ; Humans ; Insect Proteins/genetics ; Insect Vectors/*genetics/metabolism ; Male ; Membrane Transport Proteins/genetics ; Molecular Sequence Data ; Multigene Family ; Protein Structure, Tertiary/genetics ; Sequence Analysis, DNA ; Sex Characteristics ; Sex Determination Processes ; Species Specificity ; Synteny ; Transcription, Genetic ; Yellow Fever/prevention & control/transmission
    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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  • 99
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    Germ cell specification in mice (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-04-21
    Description: Specification of germ cells in mice occurs relatively late in embryonic development. It is initiated by signals that induce expression of Blimp1, a key regulator of the germ cell, in a few epiblast cells of early postimplantation embryos. Blimp1 represses the incipient somatic program in these cells and promotes progression toward the germ cell fate. Blimp1 may also have a role in the maintenance of early germ cell characteristics by ensuring their escape from the somatic fate as well as possible reversion to pluripotent stem cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hayashi, Katsuhiko -- de Sousa Lopes, Susana M Chuva -- Surani, M Azim -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2007 Apr 20;316(5823):394-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Cancer Research UK Gurdon Institute, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17446386" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Lineage ; Embryo, Mammalian/*cytology/physiology ; Embryonic Development ; Epigenesis, Genetic ; Gene Expression Regulation, Developmental ; Germ Cells/*cytology ; Mice ; Phenotype ; Pluripotent Stem Cells/cytology ; Protein Methyltransferases/genetics/physiology ; Repressor Proteins/physiology ; Transcription Factors/physiology ; Transcription, Genetic
    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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  • 100
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    An H-NS-like stealth protein aids horizontal DNA transmission in bacteria (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-01-16
    Description: The Sfh protein is encoded by self-transmissible plasmids involved in human typhoid and is closely related to the global regulator H-NS. We have found that Sfh provides a stealth function that allows the plasmids to be transmitted to new bacterial hosts with minimal effects on their fitness. Introducing the plasmid without the sfh gene imposes a mild H-NS(-) phenotype and a severe loss of fitness due to titration of the cellular pool of H-NS by the A+T-rich plasmid. This stealth strategy seems to be used widely to aid horizontal DNA transmission and has important implications for bacterial evolution.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Doyle, Marie -- Fookes, Maria -- Ivens, Al -- Mangan, Michael W -- Wain, John -- Dorman, Charles J -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2007 Jan 12;315(5809):251-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Moyne Institute of Preventive Medicine, Trinity College Dublin, Dublin 2, Ireland. cjdorman@tcd.ie〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17218529" target="_blank"〉PubMed〈/a〉
    Keywords: Bacterial Proteins/*metabolism ; *Conjugation, Genetic ; DNA-Binding Proteins/*metabolism ; Gene Expression Profiling ; Gene Expression Regulation, Bacterial ; *Gene Transfer, Horizontal ; *Genes, Bacterial ; Movement ; *Plasmids ; Salmonella typhimurium/*genetics/pathogenicity/physiology ; Shigella flexneri/*genetics ; Transcription, Genetic ; Virulence
    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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