Spt4 selectively regulates the expression of <i>C9orf72</i> sense and antisense mutant transcripts

  • Nicholas J. Kramer
    Department of Genetics, Stanford University School of Medicine, Stanford, CA, USA.
  • Yari Carlomagno
    Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.
  • Yong-Jie Zhang
    Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.
  • Sandra Almeida
    Department of Neurology, University of Massachusetts Medical School, Worcester, MA, USA.
  • Casey N. Cook
    Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.
  • Tania F. Gendron
    Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.
  • Mercedes Prudencio
    Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.
  • Marka Van Blitterswijk
    Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.
  • Veronique Belzil
    Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.
  • Julien Couthouis
    Department of Genetics, Stanford University School of Medicine, Stanford, CA, USA.
  • Joseph West Paul
    Department of Genetics, Stanford University School of Medicine, Stanford, CA, USA.
  • Lindsey D. Goodman
    Department of Biology and Neuroscience Graduate Program, University of Pennsylvania, Philadelphia, PA, USA.
  • Lillian Daughrity
    Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.
  • Jeannie Chew
    Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.
  • Aliesha Garrett
    Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.
  • Luc Pregent
    Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.
  • Karen Jansen-West
    Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.
  • Lilia J. Tabassian
    Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.
  • Rosa Rademakers
    Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.
  • Kevin Boylan
    Department of Neurology, Mayo Clinic, Jacksonville, FL, USA.
  • Neill R. Graff-Radford
    Department of Neurology, Mayo Clinic, Jacksonville, FL, USA.
  • Keith A. Josephs
    Department of Neurology, Mayo Clinic, Rochester, MN, USA.
  • Joseph E. Parisi
    Department of Neurology, Mayo Clinic, Rochester, MN, USA.
  • David S. Knopman
    Department of Neurology, Mayo Clinic, Rochester, MN, USA.
  • Ronald C. Petersen
    Department of Neurology, Mayo Clinic, Rochester, MN, USA.
  • Bradley F. Boeve
    Department of Neurology, Mayo Clinic, Rochester, MN, USA.
  • Ning Deng
    Department of Genetics, Stanford University School of Medicine, Stanford, CA, USA.
  • Yanan Feng
    Department of Genetics, Stanford University School of Medicine, Stanford, CA, USA.
  • Tzu-Hao Cheng
    Institute of Biochemistry and Molecular Biology, National Yang-Ming University, Taipei, Taiwan, Republic of China.
  • Dennis W. Dickson
    Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.
  • Stanley N. Cohen
    Department of Genetics, Stanford University School of Medicine, Stanford, CA, USA.
  • Nancy M. Bonini
    Department of Biology and Neuroscience Graduate Program, University of Pennsylvania, Philadelphia, PA, USA.
  • Christopher D. Link
    Department of Integrative Physiology, University of Colorado, Boulder, CO, USA.
  • Fen-Biao Gao
    Department of Neurology, University of Massachusetts Medical School, Worcester, MA, USA.
  • Leonard Petrucelli
    Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.
  • Aaron D. Gitler
    Department of Genetics, Stanford University School of Medicine, Stanford, CA, USA.

説明

<jats:title>Targeting three defects with one strategy</jats:title> <jats:p> The neurodegenerative diseases amyotrophic lateral sclerosis and frontotemporal dementia are most commonly caused by a mutation in the <jats:italic>C9orf72</jats:italic> gene. The mutation is an expanded hexanucleotide repeat in a noncoding region. The expanded repeat produces sense and antisense RNA transcripts, which accumulate in patient cells and appear to sequester RNA-binding proteins. The sense and antisense transcripts are also translated into dipeptide repeat proteins, which are aggregation-prone and accumulate in the brain and spinal cord. Last, loss of function from reduced expression of <jats:italic>C9orf72</jats:italic> in neurons and glia could contribute to the disease. Kramer <jats:italic>et al.</jats:italic> targeted both sense and antisense repeats by blocking a single gene called <jats:italic>SPT4</jats:italic> , which mitigated degeneration in human cells by reducing all three types of pathologies. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6300" page="708" related-article-type="in-this-issue" vol="353" xlink:href="10.1126/science.aaf7791">708</jats:related-article> </jats:p>

収録刊行物

  • Science

    Science 353 (6300), 708-712, 2016-08-12

    American Association for the Advancement of Science (AAAS)

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