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Senataxin suppresses the antiviral transcriptional response and controls viral biogenesis.

  • Author(s): Miller, Matthew S;
  • Rialdi, Alexander;
  • Ho, Jessica Sook Yuin;
  • Tilove, Micah;
  • Martinez-Gil, Luis;
  • Moshkina, Natasha P;
  • Peralta, Zuleyma;
  • Noel, Justine;
  • Melegari, Camilla;
  • Maestre, Ana M;
  • Mitsopoulos, Panagiotis;
  • Madrenas, Joaquín;
  • Heinz, Sven;
  • Benner, Chris;
  • Young, John AT;
  • Feagins, Alicia R;
  • Basler, Christopher F;
  • Fernandez-Sesma, Ana;
  • Becherel, Olivier J;
  • Lavin, Martin F;
  • van Bakel, Harm;
  • Marazzi, Ivan
  • et al.

Published Web Location

https://doi.org/10.1038/ni.3132
Abstract

The human helicase senataxin (SETX) has been linked to the neurodegenerative diseases amyotrophic lateral sclerosis (ALS4) and ataxia with oculomotor apraxia (AOA2). Here we identified a role for SETX in controlling the antiviral response. Cells that had undergone depletion of SETX and SETX-deficient cells derived from patients with AOA2 had higher expression of antiviral mediators in response to infection than did wild-type cells. Mechanistically, we propose a model whereby SETX attenuates the activity of RNA polymerase II (RNAPII) at genes stimulated after a virus is sensed and thus controls the magnitude of the host response to pathogens and the biogenesis of various RNA viruses (e.g., influenza A virus and West Nile virus). Our data indicate a potentially causal link among inborn errors in SETX, susceptibility to infection and the development of neurologic disorders.

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