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The TRPV4 channel links calcium influx to DDX3X activity and viral infectivity

Author

Listed:
  • P. Doñate-Macián

    (Universitat Pompeu Fabra
    Universitat Autònoma de Barcelona)

  • J. Jungfleisch

    (Universitat Pompeu Fabra)

  • G. Pérez-Vilaró

    (Universitat Pompeu Fabra)

  • F. Rubio-Moscardo

    (Universitat Pompeu Fabra)

  • A. Perálvarez-Marín

    (Universitat Autònoma de Barcelona)

  • J. Diez

    (Universitat Pompeu Fabra)

  • M. A. Valverde

    (Universitat Pompeu Fabra)

Abstract

Ion channels are well placed to transduce environmental cues into signals used by cells to generate a wide range of responses, but little is known about their role in the regulation of RNA metabolism. Here we show that the TRPV4 cation channel binds the DEAD-box RNA helicase DDX3X and regulates its function. TRPV4-mediated Ca2+ influx releases DDX3X from the channel and drives DDX3X nuclear translocation, a process that involves calmodulin (CaM) and the CaM-dependent kinase II. Genetic depletion or pharmacological inhibition of TRPV4 diminishes DDX3X-dependent functions, including nuclear viral export and translation. Furthermore, TRPV4 mediates Ca2+ influx and nuclear accumulation of DDX3X in cells exposed to the Zika virus or the purified viral envelope protein. Consequently, targeting of TRPV4 reduces infectivity of dengue, hepatitis C and Zika viruses. Together, our results highlight the role of TRPV4 in the regulation of DDX3X-dependent control of RNA metabolism and viral infectivity.

Suggested Citation

  • P. Doñate-Macián & J. Jungfleisch & G. Pérez-Vilaró & F. Rubio-Moscardo & A. Perálvarez-Marín & J. Diez & M. A. Valverde, 2018. "The TRPV4 channel links calcium influx to DDX3X activity and viral infectivity," Nature Communications, Nature, vol. 9(1), pages 1-13, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-04776-7
    DOI: 10.1038/s41467-018-04776-7
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