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

P. Doñate-Macián, J. Jungfleisch, G. Pérez-Vilaró, F. Rubio-Moscardo, A. Perálvarez-Marín, J. Diez and M. A. Valverde ()
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P. Doñate-Macián: Universitat Pompeu Fabra
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

Nature Communications, 2018, vol. 9, issue 1, 1-13

Abstract: 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.

Date: 2018
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DOI: 10.1038/s41467-018-04776-7

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