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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)
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    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
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  • 3
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    New neurons follow the flow of cerebrospinal fluid in the adult brain (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-01-18
    Description: In the adult brain, neuroblasts born in the subventricular zone migrate from the walls of the lateral ventricles to the olfactory bulb. How do these cells orient over such a long distance and through complex territories? Here we show that neuroblast migration parallels cerebrospinal fluid (CSF) flow. Beating of ependymal cilia is required for normal CSF flow, concentration gradient formation of CSF guidance molecules, and directional migration of neuroblasts. Results suggest that polarized epithelial cells contribute important vectorial information for guidance of young, migrating neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sawamoto, Kazunobu -- Wichterle, Hynek -- Gonzalez-Perez, Oscar -- Cholfin, Jeremy A -- Yamada, Masayuki -- Spassky, Nathalie -- Murcia, Noel S -- Garcia-Verdugo, Jose Manuel -- Marin, Oscar -- Rubenstein, John L R -- Tessier-Lavigne, Marc -- Okano, Hideyuki -- Alvarez-Buylla, Arturo -- HD 32116/HD/NICHD NIH HHS/ -- NS 28478/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2006 Feb 3;311(5761):629-32. Epub 2006 Jan 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurological Surgery and Developmental and Stem Cell Biology Program, University of California San Francisco, San Francisco, CA 94143, USA. sawamoto@sc.itc.keio.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16410488" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Tissue Transplantation ; Cell Movement ; Cell Polarity ; Cerebral Ventricles/cytology/physiology ; Cerebrospinal Fluid/*physiology ; Choroid Plexus/secretion ; Cilia/physiology ; Ependyma/cytology/*physiology ; Epithelial Cells/physiology ; Intercellular Signaling Peptides and Proteins ; Mice ; Nerve Tissue Proteins/cerebrospinal fluid ; Neurons/cytology/*physiology ; Olfactory Bulb/cytology/physiology ; Recombinant Fusion Proteins/cerebrospinal fluid
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Evolutionarily dynamic alternative splicing of GPR56 regulates regional cerebral cortical patterning (2014)
    American Association for the Advancement of Science (AAAS)
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    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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    Role of inositol 1,4,5-trisphosphate receptor in ventral signaling in Xenopus embryos (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-01-07
    Description: The inositol 1,4,5-trisphosphate (IP3) receptor is a calcium ion channel involved in the release of free Ca2+ from intracellular stores. For analysis of the role of IP3-induced Ca2+ release (IICR) on patterning of the embryonic body, monoclonal antibodies that inhibit IICR were produced. Injection of these blocking antibodies into the ventral part of early Xenopus embryos induced modest dorsal differentiation. A close correlation between IICR blocking potencies and ectopic dorsal axis induction frequency suggests that an active IP3-Ca2+ signal may participate in the modulation of ventral differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kume, S -- Muto, A -- Inoue, T -- Suga, K -- Okano, H -- Mikoshiba, K -- New York, N.Y. -- Science. 1997 Dec 12;278(5345):1940-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mikoshiba Calciosignal Net Project, Exploratory Research for Advanced Technology (ERATO), Japan Science and Technology Corporation (JST), 2-9-3 Shimo-Meguro, Meguro-ku, Tokyo 153, Japan. skume@ims.u-tokyo.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9395395" target="_blank"〉PubMed〈/a〉
    Keywords: Activins ; Animals ; Antibodies, Blocking ; Antibodies, Monoclonal ; *Body Patterning ; Calcium/*metabolism ; Calcium Channels/immunology/*metabolism ; Cell Differentiation ; Embryo, Nonmammalian/*metabolism ; Embryonic Development ; Embryonic Induction ; Fibroblast Growth Factor 2/pharmacology ; Gastrula/metabolism ; Gene Expression Regulation, Developmental ; Inhibins/pharmacology ; Inositol 1,4,5-Trisphosphate/*metabolism ; Inositol 1,4,5-Trisphosphate Receptors ; Receptors, Cytoplasmic and Nuclear/immunology/*metabolism ; *Signal Transduction ; Xenopus
    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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    Loss of imprinting of Igf2 alters intestinal maturation and tumorigenesis in mice (2005)
    American Association for the Advancement of Science (AAAS)
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    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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  • 7
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    Sema3A regulates bone-mass accrual through sensory innervations (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-05-07
    Description: Semaphorin 3A (Sema3A) is a diffusible axonal chemorepellent that has an important role in axon guidance. Previous studies have demonstrated that Sema3a(-/-) mice have multiple developmental defects due to abnormal neuronal innervations. Here we show in mice that Sema3A is abundantly expressed in bone, and cell-based assays showed that Sema3A affected osteoblast differentiation in a cell-autonomous fashion. Accordingly, Sema3a(-/-) mice had a low bone mass due to decreased bone formation. However, osteoblast-specific Sema3A-deficient mice (Sema3acol1(-/-) and Sema3aosx(-/-) mice) had normal bone mass, even though the expression of Sema3A in bone was substantially decreased. In contrast, mice lacking Sema3A in neurons (Sema3asynapsin(-/-) and Sema3anestin(-/-) mice) had low bone mass, similar to Sema3a(-/-) mice, indicating that neuron-derived Sema3A is responsible for the observed bone abnormalities independent of the local effect of Sema3A in bone. Indeed, the number of sensory innervations of trabecular bone was significantly decreased in Sema3asynapsin(-/-) mice, whereas sympathetic innervations of trabecular bone were unchanged. Moreover, ablating sensory nerves decreased bone mass in wild-type mice, whereas it did not reduce the low bone mass in Sema3anestin(-/-) mice further, supporting the essential role of the sensory nervous system in normal bone homeostasis. Finally, neuronal abnormalities in Sema3a(-/-) mice, such as olfactory development, were identified in Sema3asynasin(-/-) mice, demonstrating that neuron-derived Sema3A contributes to the abnormal neural development seen in Sema3a(-/-) mice, and indicating that Sema3A produced in neurons regulates neural development in an autocrine manner. This study demonstrates that Sema3A regulates bone remodelling indirectly by modulating sensory nerve development, but not directly by acting on osteoblasts.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fukuda, Toru -- Takeda, Shu -- Xu, Ren -- Ochi, Hiroki -- Sunamura, Satoko -- Sato, Tsuyoshi -- Shibata, Shinsuke -- Yoshida, Yutaka -- Gu, Zirong -- Kimura, Ayako -- Ma, Chengshan -- Xu, Cheng -- Bando, Waka -- Fujita, Koji -- Shinomiya, Kenichi -- Hirai, Takashi -- Asou, Yoshinori -- Enomoto, Mitsuhiro -- Okano, Hideyuki -- Okawa, Atsushi -- Itoh, Hiroshi -- NS065048/NS/NINDS NIH HHS/ -- England -- Nature. 2013 May 23;497(7450):490-3. doi: 10.1038/nature12115. Epub 2013 May 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, School of Medicine, Keio University, Shinanomachi 35, Shinjyuku-ku, Tokyo 160-8582, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23644455" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Bone Remodeling ; Bone and Bones/anatomy & histology/*innervation/*metabolism ; Cell Differentiation ; Cells, Cultured ; Female ; Male ; Mice ; Organ Size ; Osteoblasts/cytology/metabolism ; Semaphorin-3A/deficiency/genetics/*metabolism ; Sensory Receptor Cells/cytology/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
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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
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