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  • 1
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    Generation of transgenic non-human primates with germline transmission (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-05-30
    Description: The common marmoset (Callithrix jacchus) is increasingly attractive for use as a non-human primate animal model in biomedical research. It has a relatively high reproduction rate for a primate, making it potentially suitable for transgenic modification. Although several attempts have been made to produce non-human transgenic primates, transgene expression in the somatic tissues of live infants has not been demonstrated by objective analyses such as polymerase chain reaction with reverse transcription or western blots. Here we show that the injection of a self-inactivating lentiviral vector in sucrose solution into marmoset embryos results in transgenic common marmosets that expressed the transgene in several organs. Notably, we achieved germline transmission of the transgene, and the transgenic offspring developed normally. The successful creation of transgenic marmosets provides a new animal model for human disease that has the great advantage of a close genetic relationship with humans. This model will be valuable to many fields of biomedical research.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sasaki, Erika -- Suemizu, Hiroshi -- Shimada, Akiko -- Hanazawa, Kisaburo -- Oiwa, Ryo -- Kamioka, Michiko -- Tomioka, Ikuo -- Sotomaru, Yusuke -- Hirakawa, Reiko -- Eto, Tomoo -- Shiozawa, Seiji -- Maeda, Takuji -- Ito, Mamoru -- Ito, Ryoji -- Kito, Chika -- Yagihashi, Chie -- Kawai, Kenji -- Miyoshi, Hiroyuki -- Tanioka, Yoshikuni -- Tamaoki, Norikazu -- Habu, Sonoko -- Okano, Hideyuki -- Nomura, Tatsuji -- England -- Nature. 2009 May 28;459(7246):523-7. doi: 10.1038/nature08090.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Central Institute for Experimental Animals, 1430 Nogawa, Miyamae-ku, Kawasaki, Kanagawa 216-0001, Japan. esasaki@ciea.or.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19478777" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified/*genetics ; Animals, Newborn ; Callithrix/embryology/*genetics ; *Disease Models, Animal ; Gene Expression Profiling ; Germ Cells/*metabolism ; Green Fluorescent Proteins/genetics ; Heredity/*genetics ; Humans ; Transcription, Genetic ; Transgenes/*genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    Identification of UBIAD1 as a novel human menaquinone-4 biosynthetic enzyme (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-10-19
    Description: Vitamin K occurs in the natural world in several forms, including a plant form, phylloquinone (PK), and a bacterial form, menaquinones (MKs). In many species, including humans, PK is a minor constituent of hepatic vitamin K content, with most hepatic vitamin K content comprising long-chain MKs. Menaquinone-4 (MK-4) is ubiquitously present in extrahepatic tissues, with particularly high concentrations in the brain, kidney and pancreas of humans and rats. It has consistently been shown that PK is endogenously converted to MK-4 (refs 4-8). This occurs either directly within certain tissues or by interconversion to menadione (K(3)), followed by prenylation to MK-4 (refs 9-12). No previous study has sought to identify the human enzyme responsible for MK-4 biosynthesis. Previously we provided evidence for the conversion of PK and K(3) into MK-4 in mouse cerebra. However, the molecular mechanisms for these conversion reactions are unclear. Here we identify a human MK-4 biosynthetic enzyme. We screened the human genome database for prenylation enzymes and found UbiA prenyltransferase containing 1 (UBIAD1), a human homologue of Escherichia coli prenyltransferase menA. We found that short interfering RNA against the UBIAD1 gene inhibited the conversion of deuterium-labelled vitamin K derivatives into deuterium-labelled-MK-4 (MK-4-d(7)) in human cells. We confirmed that the UBIAD1 gene encodes an MK-4 biosynthetic enzyme through its expression and conversion of deuterium-labelled vitamin K derivatives into MK-4-d(7) in insect cells infected with UBIAD1 baculovirus. Converted MK-4-d(7) was chemically identified by (2)H-NMR analysis. MK-4 biosynthesis by UBIAD1 was not affected by the vitamin K antagonist warfarin. UBIAD1 was localized in endoplasmic reticulum and ubiquitously expressed in several tissues of mice. Our results show that UBIAD1 is a human MK-4 biosynthetic enzyme; this identification will permit more effective decisions to be made about vitamin K intake and bone health.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakagawa, Kimie -- Hirota, Yoshihisa -- Sawada, Natsumi -- Yuge, Naohito -- Watanabe, Masato -- Uchino, Yuri -- Okuda, Naoko -- Shimomura, Yuka -- Suhara, Yoshitomo -- Okano, Toshio -- England -- Nature. 2010 Nov 4;468(7320):117-21. doi: 10.1038/nature09464. Epub 2010 Oct 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Hygienic Sciences, Kobe Pharmaceutical University, 4-19-1, Motoyamakita-machi, Higashinada-ku, Kobe 658-8558, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20953171" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Baculoviridae/genetics/physiology ; Bone and Bones/metabolism ; Cell Line ; Dimethylallyltranstransferase ; Humans ; Magnetic Resonance Imaging ; Mice ; Osteoblasts ; Proteins/genetics/*metabolism ; RNA, Small Interfering/genetics/metabolism ; Spodoptera/cytology/virology ; Vitamin K/antagonists & inhibitors/metabolism ; Vitamin K 1/metabolism ; Vitamin K 2/*analogs & derivatives/analysis/chemistry/metabolism ; Warfarin/pharmacology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    Evolutionary dynamics of complex networks of HIV drug-resistant strains: the case of San Francisco (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-01-16
    Description: Over the past two decades, HIV resistance to antiretroviral drugs (ARVs) has risen to high levels in the wealthier countries of the world, which are able to afford widespread treatment. We have gained insights into the evolution and transmission dynamics of ARV resistance by designing a biologically complex multistrain network model. With this model, we traced the evolutionary history of ARV resistance in San Francisco and predict its future dynamics. By using classification and regression trees, we identified the key immunologic, virologic, and treatment factors that increase ARV resistance. Our modeling shows that 60% of the currently circulating ARV-resistant strains in San Francisco are capable of causing self-sustaining epidemics, because each individual infected with one of these strains can cause, on average, more than one new resistant infection. It is possible that a new wave of ARV-resistant strains that pose a substantial threat to global public health is emerging.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, Robert J -- Okano, Justin T -- Kahn, James S -- Bodine, Erin N -- Blower, Sally -- K24RR024369/RR/NCRR NIH HHS/ -- P30-AI27763/AI/NIAID NIH HHS/ -- R01 AI041935/AI/NIAID NIH HHS/ -- R18-HS017784/HS/AHRQ HHS/ -- New York, N.Y. -- Science. 2010 Feb 5;327(5966):697-701. doi: 10.1126/science.1180556. Epub 2010 Jan 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Biomedical Modeling, Semel Institute of Neuroscience & Human Behavior, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA 90024, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20075214" target="_blank"〉PubMed〈/a〉
    Keywords: Anti-HIV Agents/*pharmacology/therapeutic use ; Antiretroviral Therapy, Highly Active ; Computer Simulation ; Disease Outbreaks ; Drug Resistance, Multiple, Viral ; *Drug Resistance, Viral ; Drug Therapy, Combination ; Evolution, Molecular ; Forecasting ; HIV/*drug effects/genetics ; HIV Infections/drug therapy/epidemiology/*transmission/*virology ; HIV Protease Inhibitors/pharmacology/therapeutic use ; Homosexuality, Male ; Humans ; Male ; Models, Statistical ; Monte Carlo Method ; Probability ; Reverse Transcriptase Inhibitors/pharmacology/therapeutic use ; San Francisco/epidemiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 4
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    Evolutionarily dynamic alternative splicing of GPR56 regulates regional cerebral cortical patterning (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-02-18
    Description: The human neocortex has numerous specialized functional areas whose formation is poorly understood. Here, we describe a 15-base pair deletion mutation in a regulatory element of GPR56 that selectively disrupts human cortex surrounding the Sylvian fissure bilaterally including "Broca's area," the primary language area, by disrupting regional GPR56 expression and blocking RFX transcription factor binding. GPR56 encodes a heterotrimeric guanine nucleotide-binding protein (G protein)-coupled receptor required for normal cortical development and is expressed in cortical progenitor cells. GPR56 expression levels regulate progenitor proliferation. GPR56 splice forms are highly variable between mice and humans, and the regulatory element of gyrencephalic mammals directs restricted lateral cortical expression. Our data reveal a mechanism by which control of GPR56 expression pattern by multiple alternative promoters can influence stem cell proliferation, gyral patterning, and, potentially, neocortex evolution.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4480613/" 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/PMC4480613/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bae, Byoung-Il -- Tietjen, Ian -- Atabay, Kutay D -- Evrony, Gilad D -- Johnson, Matthew B -- Asare, Ebenezer -- Wang, Peter P -- Murayama, Ayako Y -- Im, Kiho -- Lisgo, Steven N -- Overman, Lynne -- Sestan, Nenad -- Chang, Bernard S -- Barkovich, A James -- Grant, P Ellen -- Topcu, Meral -- Politsky, Jeffrey -- Okano, Hideyuki -- Piao, Xianhua -- Walsh, Christopher A -- 2R01NS035129/NS/NINDS NIH HHS/ -- G0700089/Medical Research Council/United Kingdom -- GR082557/Wellcome Trust/United Kingdom -- HHSN275200900011C/PHS HHS/ -- N01-HD-9-0011/HD/NICHD NIH HHS/ -- R01 NS035129/NS/NINDS NIH HHS/ -- U01 MH081896/MH/NIMH NIH HHS/ -- U01MH081896/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Feb 14;343(6172):764-8. doi: 10.1126/science.1244392.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Genetics and Genomics, Manton Center for Orphan Disease, and Howard Hughes Medical Institute, Boston Children's Hospital, Broad Institute of MIT and Harvard, and Departments of Pediatrics and Neurology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24531968" target="_blank"〉PubMed〈/a〉
    Keywords: *Alternative Splicing ; Animals ; Base Sequence ; Biological Evolution ; Body Patterning/*genetics ; Cats ; Cell Proliferation ; Cerebral Cortex/anatomy & histology/cytology/*embryology ; Codon, Nonsense ; Frontal Lobe/anatomy & histology/cytology/embryology ; Genetic Variation ; Haplotypes ; Humans ; Mice ; Molecular Sequence Data ; Neural Stem Cells/cytology/*physiology ; Pedigree ; Promoter Regions, Genetic/genetics ; Receptors, G-Protein-Coupled/*genetics ; Sequence Deletion
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Loss of imprinting of Igf2 alters intestinal maturation and tumorigenesis in mice (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-02-26
    Description: Loss of imprinting (LOI) of the insulin-like growth factor II gene (IGF2) is an epigenetic alteration that results in a modest increase in IGF2 expression, and it is present in the normal colonic mucosa of about 30% of patients with colorectal cancer. To investigate its role in intestinal tumorigenesis, we created a mouse model of Igf2 LOI by crossing female H19+/- mice with male Apc+/Min mice. Mice with LOI developed twice as many intestinal tumors as did control littermates. Notably, these mice also showed a shift toward a less differentiated normal intestinal epithelium, reflected by an increase in crypt length and increased staining with progenitor cell markers. A similar shift in differentiation was seen in the normal colonic mucosa of humans with LOI. Thus, altered maturation of nonneoplastic tissue may be one mechanism by which epigenetic changes affect cancer risk.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sakatani, Takashi -- Kaneda, Atsushi -- Iacobuzio-Donahue, Christine A -- Carter, Mark G -- de Boom Witzel, Sten -- Okano, Hideyuki -- Ko, Minoru S H -- Ohlsson, Rolf -- Longo, Dan L -- Feinberg, Andrew P -- K08CA106610/CA/NCI NIH HHS/ -- R01CA65145/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2005 Mar 25;307(5717):1976-8. Epub 2005 Feb 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of 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/15731405" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoma/etiology/pathology ; Animals ; Apoptosis ; Cell Differentiation ; Cell Proliferation ; Colon/cytology/metabolism ; Colonic Neoplasms/etiology/pathology ; Enterocytes/*cytology/metabolism ; Ephrin-B1/analysis ; Epigenesis, Genetic ; Female ; *Genomic Imprinting ; Humans ; Insulin-Like Growth Factor II/*genetics/*metabolism ; Intestinal Mucosa/*cytology/metabolism ; Intestinal Neoplasms/*etiology/pathology ; Intestines/*metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Microfilament Proteins/analysis ; Nerve Tissue Proteins/analysis ; Nuclear Proteins/analysis ; RNA, Long Noncoding ; RNA, Untranslated/genetics ; RNA-Binding Proteins/analysis ; Stem Cells/cytology ; Transcription Factors/analysis ; Twist Transcription Factor
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    DISC1-dependent switch from progenitor proliferation to migration in the developing cortex (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-04-08
    Description: Regulatory mechanisms governing the sequence from progenitor cell proliferation to neuronal migration during corticogenesis are poorly understood. Here we report that phosphorylation of DISC1, a major susceptibility factor for several mental disorders, acts as a molecular switch from maintaining proliferation of mitotic progenitor cells to activating migration of postmitotic neurons in mice. Unphosphorylated DISC1 regulates canonical Wnt signalling via an interaction with GSK3beta, whereas specific phosphorylation at serine 710 (S710) triggers the recruitment of Bardet-Biedl syndrome (BBS) proteins to the centrosome. In support of this model, loss of BBS1 leads to defects in migration, but not proliferation, whereas DISC1 knockdown leads to deficits in both. A phospho-dead mutant can only rescue proliferation, whereas a phospho-mimic mutant rescues exclusively migration defects. These data highlight a dual role for DISC1 in corticogenesis and indicate that phosphorylation of this protein at S710 activates a key developmental switch.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3088774/" 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/PMC3088774/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ishizuka, Koko -- Kamiya, Atsushi -- Oh, Edwin C -- Kanki, Hiroaki -- Seshadri, Saurav -- Robinson, Jon F -- Murdoch, Hannah -- Dunlop, Allan J -- Kubo, Ken-ichiro -- Furukori, Keiko -- Huang, Beverly -- Zeledon, Mariela -- Hayashi-Takagi, Akiko -- Okano, Hideyuki -- Nakajima, Kazunori -- Houslay, Miles D -- Katsanis, Nicholas -- Sawa, Akira -- DK-072301/DK/NIDDK NIH HHS/ -- DK-075972/DK/NIDDK NIH HHS/ -- G0600765/Medical Research Council/United Kingdom -- HD-04260/HD/NICHD NIH HHS/ -- MH-069853/MH/NIMH NIH HHS/ -- MH-084018/MH/NIMH NIH HHS/ -- MH-085226/MH/NIMH NIH HHS/ -- MH-088753/MH/NIMH NIH HHS/ -- MH-091230/MH/NIMH NIH HHS/ -- R01 DK072301/DK/NIDDK NIH HHS/ -- R01 DK075972/DK/NIDDK NIH HHS/ -- R01 DK075972-06/DK/NIDDK NIH HHS/ -- R01 HD042601/HD/NICHD NIH HHS/ -- R01 HD042601-10/HD/NICHD NIH HHS/ -- R01 MH091230/MH/NIMH NIH HHS/ -- R01 MH092443/MH/NIMH NIH HHS/ -- England -- Nature. 2011 May 5;473(7345):92-6. doi: 10.1038/nature09859. Epub 2011 Apr 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21471969" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; COS Cells ; Cell Movement/genetics ; Cell Proliferation ; Cercopithecus aethiops ; Cerebral Cortex/cytology/*embryology/physiology ; Gene Knockdown Techniques ; Glycogen Synthase Kinase 3/metabolism ; HEK293 Cells ; Humans ; Mice ; Microtubule-Associated Proteins/genetics/metabolism ; *Nerve Tissue Proteins/genetics/metabolism ; Neurons/*cytology/metabolism/*physiology ; PC12 Cells ; Phosphorylation ; Protein Binding ; Rats ; Signal Transduction ; Stem Cells/*cytology ; Wnt Proteins/metabolism ; beta Catenin/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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