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  • 1
    Publication Date: 2016-03-24
    Description: Lytic to temperate switching of viral communities Nature 531, 7595 (2016). doi:10.1038/nature17193 Authors: B. Knowles, C. B. Silveira, B. A. Bailey, K. Barott, V. A. Cantu, A. G. Cobián-Güemes, F. H. Coutinho, E. A. Dinsdale, B. Felts, K. A. Furby, E. E. George, K. T. Green, G. B. Gregoracci, A. F. Haas, J. M. Haggerty, E. R. Hester, N. Hisakawa, L. W. Kelly, Y. W. Lim, M. Little, A. Luque, T. McDole-Somera, K. McNair, L. S. de Oliveira, S. D. Quistad, N. L. Robinett, E. Sala, P. Salamon, S. E. Sanchez, S. Sandin, G. G. Z. Silva, J. Smith, C. Sullivan, C. Thompson, M. J. A. Vermeij, M. Youle, C. Young, B. Zgliczynski, R. Brainard, R. A. Edwards, J. Nulton, F. Thompson & F. Rohwer Microbial viruses can control host abundances via density-dependent lytic predator–prey dynamics. Less clear is how temperate viruses, which coexist and replicate with their host, influence microbial communities. Here we show that virus-like particles are relatively less abundant at high host densities. This suggests suppressed lysis
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Springer Nature
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  • 2
    Publication Date: 2015-05-24
    Description: Biochemistry DOI: 10.1021/acs.biochem.5b00246
    Print ISSN: 0006-2960
    Electronic ISSN: 1520-4995
    Topics: Biology , Chemistry and Pharmacology
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  • 3
    Publication Date: 1989-04-28
    Description: Mice transgenic for a hybrid gene containing the liver promoter of the mouse amylase gene (Amy-1a) fused to the SV40 tumor antigen coding region unexpected developed malignant brown adipose tissue tumors (malignant hibernomas). Expression of the alpha-amylase gene had previously been thought to be confined to the liver parotid, and pancreas; however, analysis of white and brown adipose tissue from nontransgenic mice revealed expression of the endogenous Amy-1a gene in these tissues. Gene constructs driven by the Amy-1a liver promoter thus provide a means of targeting gene expression to the adipocyte cell lineage in transgenic mice. Moreover the high frequency of metastases in the liver, lungs, spleen, heart, and adrenals of these mice provides an experimental system in which to study the development of disseminated malignancy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fox, N -- Crooke, R -- Hwang, L H -- Schibler, U -- Knowles, B B -- Solter, D -- CA-10815/CA/NCI NIH HHS/ -- CA-18470/CA/NCI NIH HHS/ -- CA-21124/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1989 Apr 28;244(4903):460-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wistar Institute, Philadelphia, PA 19104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2785714" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/metabolism/pathology ; *Adipose Tissue, Brown/metabolism/pathology ; Animals ; Antigens, Polyomavirus Transforming/*genetics ; Cloning, Molecular ; Gene Expression Regulation ; Liver/metabolism ; Mice ; Mice, Transgenic ; Neoplasm Metastasis ; Neoplasms, Experimental/*genetics/pathology ; Nucleic Acid Hybridization ; Promoter Regions, Genetic ; RNA, Messenger/metabolism ; Tissue Distribution ; Transcription, Genetic ; alpha-Amylases/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2012-03-24
    Description: Phenotypic variability in genetic disease is usually attributed to genetic background variation or environmental influence. Here, we show that deletion of a single gene, Trim28 (Kap1 or Tif1beta), from the maternal germ line alone, on an otherwise identical genetic background, results in severe phenotypic and epigenetic variability that leads to embryonic lethality. We identify early and minute epigenetic variations in blastomeres of the preimplantation embryo of these animals, suggesting that the embryonic lethality may result from the misregulation of genomic imprinting in mice lacking maternal Trim28. Our results reveal the long-range effects of a maternal gene deletion on epigenetic memory and illustrate the delicate equilibrium of maternal and zygotic factors during nuclear reprogramming.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Messerschmidt, Daniel M -- de Vries, Wilhelmine -- Ito, Mitsuteru -- Solter, Davor -- Ferguson-Smith, Anne -- Knowles, Barbara B -- 079249/Wellcome Trust/United Kingdom -- 095606/Wellcome Trust/United Kingdom -- MR/J001597/1/Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2012 Mar 23;335(6075):1499-502. doi: 10.1126/science.1216154.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mammalian Development Group, Institute of Medical Biology, Singapore.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22442485" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/physiology ; DNA Methylation ; Down-Regulation ; *Embryo Loss ; Embryo, Mammalian/*physiology ; Embryonic Development ; *Epigenesis, Genetic ; Female ; Gene Expression Regulation, Developmental ; *Genomic Imprinting ; Insulin-Like Growth Factor II/genetics/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Nuclear Proteins/*genetics/*physiology ; Oligonucleotide Array Sequence Analysis ; Oocytes/*physiology ; Phenotype ; RNA, Long Noncoding ; RNA, Untranslated/genetics/metabolism ; Repressor Proteins/*genetics/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2004-12-14
    Description: Mammalian oocytes are held in prophase arrest by an unknown signal from the surrounding somatic cells. Here we show that the orphan Gs-linked receptor GPR3, which is localized in the oocyte, maintains this arrest. Oocytes from Gpr3 knockout mice resume meiosis within antral follicles, independently of an increase in luteinizing hormone, and this phenotype can be reversed by injection of Gpr3 RNA into the oocytes. Thus, the GPR3 receptor is a link in communication between the somatic cells and oocyte of the ovarian follicle and is crucial for the regulation of meiosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mehlmann, Lisa M -- Saeki, Yoshinaga -- Tanaka, Shigeru -- Brennan, Thomas J -- Evsikov, Alexei V -- Pendola, Frank L -- Knowles, Barbara B -- Eppig, John J -- Jaffe, Laurinda A -- New York, N.Y. -- Science. 2004 Dec 10;306(5703):1947-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, University of Connecticut Health Center (UCHC), Farmington, CT 06032, USA. lmehlmann@neuron.uchc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15591206" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclases/metabolism ; Animals ; Chondroitin Sulfate Proteoglycans/genetics/metabolism ; Expressed Sequence Tags ; Female ; Granulosa Cells/physiology ; Heterotrimeric GTP-Binding Proteins/*metabolism ; In Situ Hybridization ; Lectins, C-Type ; Ligands ; Luteinizing Hormone/metabolism ; *Meiosis ; Metaphase ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mitosis ; Oocytes/*physiology ; Ovarian Follicle/*physiology ; RNA/genetics/metabolism ; Receptors, G-Protein-Coupled/genetics/*physiology ; Versicans
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 2013-09-07
    Description: Epigenetic alterations are increasingly recognized as causes of human cancers and disease. These aberrations are likely to arise during genomic reprogramming in mammalian preimplantation embryos, when their epigenomes are most vulnerable. However, this process is only partially understood because of the experimental inaccessibility of early-stage embryos. Here, we introduce a methodologic advance, probing single cells for various DNA-methylation errors at multiple loci, to reveal failed maintenance of epigenetic mark results in chimeric mice, which display unpredictable phenotypes leading to developmental arrest. Yet we show that mouse pronuclear transfer can be used to ameliorate such reprogramming defects. This study not only details the epigenetic reprogramming dynamics in early mammalian embryos but also suggests diagnostic and potential future therapeutic applications.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lorthongpanich, Chanchao -- Cheow, Lih Feng -- Balu, Sathish -- Quake, Stephen R -- Knowles, Barbara B -- Burkholder, William F -- Solter, Davor -- Messerschmidt, Daniel M -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Sep 6;341(6150):1110-2. doi: 10.1126/science.1240617.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mammalian Development Group, Institute of Medical Biology, A*STAR, Singapore.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24009393" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/*metabolism ; Cellular Reprogramming/*genetics ; *Chimerism ; *DNA Methylation ; *Epigenesis, Genetic ; Gene Deletion ; *Gene Expression Regulation, Developmental ; Genetic Loci ; Humans ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Nuclear Proteins/genetics ; Repressor Proteins/genetics ; Single-Cell Analysis
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2016-11-03
    Description: Corrigendum: Lytic to temperate switching of viral communities Nature 539, 7627 (2016). doi:10.1038/nature19335 Authors: B. Knowles, C. B. Silveira, B. A. Bailey, K. Barott, V. A. Cantu, A. G. Cobián-Güemes, F. H. Coutinho, E. A. Dinsdale, B. Felts, K. A. Furby, E. E. George, K. T. Green, G. B. Gregoracci, A. F. Haas, J. M. Haggerty, E. R. Hester, N. Hisakawa, L. W. Kelly, Y. W. Lim, M. Little, A. Luque, T. McDole-Somera, K. McNair, L. S. de Oliveira, S. D. Quistad, N. L. Robinett, E. Sala, P. Salamon, S. E. Sanchez, S. Sandin, G. G. Z. Silva, J. Smith, C. Sullivan, C. Thompson, M. J. A. Vermeij, M. Youle, C. Young, B. Zgliczynski, R. Brainard, R. A. Edwards, J. Nulton, F. Thompson & F. Rohwer Nature531, 466–470 (2016); doi:10.1038/nature17193In this Article, the ‘Predator–prey modelling’ section of the Methods shows Lotka–Volterra equations. Although these equations are meant to present a basic Lotka–Volterra model, the term ‘N/K’ in the
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Springer Nature
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  • 8
    Publication Date: 2016-03-17
    Description: Microbial viruses can control host abundances via density-dependent lytic predator-prey dynamics. Less clear is how temperate viruses, which coexist and replicate with their host, influence microbial communities. Here we show that virus-like particles are relatively less abundant at high host densities. This suggests suppressed lysis where established models predict lytic dynamics are favoured. Meta-analysis of published viral and microbial densities showed that this trend was widespread in diverse ecosystems ranging from soil to freshwater to human lungs. Experimental manipulations showed viral densities more consistent with temperate than lytic life cycles at increasing microbial abundance. An analysis of 24 coral reef viromes showed a relative increase in the abundance of hallmark genes encoded by temperate viruses with increased microbial abundance. Based on these four lines of evidence, we propose the Piggyback-the-Winner model wherein temperate dynamics become increasingly important in ecosystems with high microbial densities; thus 'more microbes, fewer viruses'.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Knowles, B -- Silveira, C B -- Bailey, B A -- Barott, K -- Cantu, V A -- Cobian-Guemes, A G -- Coutinho, F H -- Dinsdale, E A -- Felts, B -- Furby, K A -- George, E E -- Green, K T -- Gregoracci, G B -- Haas, A F -- Haggerty, J M -- Hester, E R -- Hisakawa, N -- Kelly, L W -- Lim, Y W -- Little, M -- Luque, A -- McDole-Somera, T -- McNair, K -- de Oliveira, L S -- Quistad, S D -- Robinett, N L -- Sala, E -- Salamon, P -- Sanchez, S E -- Sandin, S -- Silva, G G Z -- Smith, J -- Sullivan, C -- Thompson, C -- Vermeij, M J A -- Youle, M -- Young, C -- Zgliczynski, B -- Brainard, R -- Edwards, R A -- Nulton, J -- Thompson, F -- Rohwer, F -- England -- Nature. 2016 Mar 24;531(7595):466-70. doi: 10.1038/nature17193. Epub 2016 Mar 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, San Diego State University, 5500 Campanile Drive, San Diego, California 92182, USA. ; Biology Institute, Rio de Janeiro Federal University, Av. Carlos Chagas Filho 373, Rio de Janeiro, Rio de Janeiro 21941-599, Brazil. ; Department of Mathematics and Statistics, San Diego State University, 5500 Campanile Drive, San Diego, California 92182, USA. ; Hawaii Institute of Marine Biology, University of Hawaii at Manoa, 46-007 Lilipuna Road, Kaneohe, Hawaii 96744, USA. ; Computational Science Research Center, San Diego State University, 5500 Campanile Drive, San Diego, California 92182, USA. ; Rainbow Rock, Ocean View, Hawaii 96737, USA. ; Radboud University Medical Centre, Radboud Institute for Molecular Life Sciences, Centre for Molecular and Biomolecular Informatics, 6525HP Nijmegen, The Netherlands. ; Viral Information Institute, San Diego State University, 5500 Campanile Drive, San Diego, California 92182, USA. ; Scripps Institution of Oceanography, 8622 Kennel Way, La Jolla, California 92037, USA. ; Department of Biology, University of California San Diego, 9500 Gilman Drive, La Jolla, California 92093, USA. ; Marine Sciences Department, Sao Paulo Federal University - Baixada Santista, Av. Alm. Saldanha da Gama, 89, Santos, Sao Paulo 11030-400, Brazil. ; National Geographic Society, 1145 17th St NW, Washington D.C. 20036, USA. ; CARMABI Foundation, Piscaderabaai z/n, Willemstad, Curacao, Netherlands Antilles. ; Aquatic Microbiology, Institute for Biodiversity and Ecosystem Dynamics, University of Amsterdam, 1098XH Amsterdam, The Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26982729" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anthozoa/physiology/*virology ; Bacteriophages/pathogenicity/physiology ; Coral Reefs ; *Ecosystem ; Genes, Viral/genetics ; *Host-Pathogen Interactions ; Lysogeny ; Models, Biological ; Virulence/genetics ; Viruses/genetics/isolation & purification/*pathogenicity
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    Electronic ISSN: 1476-4687
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  • 9
    Publication Date: 1982-01-22
    Description: A 180,000-dalton single-chain molecule (human pro-C3) is the precursor of the third component of human complement (C3), a disulfide-linked two-chain protein. The pro-C3 is converted by limited proteolysis to C3. The relationship between pro-C3 and C3 was established with the use of Hep G2, a cell line derived from a human hepatocellular carcinoma, which synthesizes at least 17 plasma proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morris, K M -- Goldberger, G -- Colten, H R -- Aden, D P -- Knowles, B B -- AM 16392/AM/NIADDK NIH HHS/ -- CA 18470/CA/NCI NIH HHS/ -- CA 25875/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1982 Jan 22;215(4531):399-400.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7199205" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Complement C3/*biosynthesis ; Humans ; Liver Neoplasms, Experimental/*metabolism ; Macromolecular Substances ; Molecular Weight ; Protein Precursors/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 1980-07-25
    Description: Analysis of the cell culture fluid from two new human hepatoma-derived cell lines reveals that 17 of the major human plasma proteins are synthesized and secreted by these cells. One of these cell lines, Hep 3B, also produces the two major polypeptides of the hepatitis B virus surface antigen. When Hep 3B in injected into athymic mice, metastatic hepatocellular carcinomas appear. These cell lines provide experimental models for investigation of plasma protein biosynthesis and the relation of the hepatitis B viru genome to tumorigenicity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Knowles, B B -- Howe, C C -- Aden, D P -- New York, N.Y. -- Science. 1980 Jul 25;209(4455):497-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6248960" target="_blank"〉PubMed〈/a〉
    Keywords: Blood Proteins/*secretion ; Carcinoma, Hepatocellular/immunology/*secretion ; Cell Line ; Electrophoresis, Polyacrylamide Gel ; Hepatitis B Surface Antigens/*analysis ; Humans ; Immunodiffusion ; Liver Neoplasms/immunology/*secretion
    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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