Published in

Rockefeller University Press, Journal of Cell Biology, 3(182), p. 437-447, 2008

DOI: 10.1083/jcb.200805124

Rockefeller University Press, Journal of General Physiology, 3(132), p. i2-i2

DOI: 10.1085/jgp1323oia2

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TRPP2 and TRPV4 form a polymodal sensory channel complex

Journal article published in 2008 by Michael Köttgen, E. Wolfgang Kuehn, Michael Kottgen, Bj Buchholz, Miguel A. Garcia-Gonzalez, Fruzsina Kotsis, Xiao Fu, Mara Doerken, Christopher Boehlke, Daniel Steffl, Robert Tauber, Tomasz Wegierski, Roland Nitschke ORCID, Makoto Suzuki, Albrecht Kramer-Zucker and other authors.
This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Abstract

The primary cilium has evolved as a multifunctional cellular compartment that decorates most vertebrate cells. Cilia sense mechanical stimuli in various organs, but the molecular mechanisms that convert the deflection of cilia into intracellular calcium transients have remained elusive. Polycystin-2 (TRPP2), an ion channel mutated in polycystic kidney disease, is required for cilia-mediated calcium transients but lacks mechanosensitive properties. We find here that TRPP2 utilizes TRPV4 to form a mechano- and thermosensitive molecular sensor in the cilium. Depletion of TRPV4 in renal epithelial cells abolishes flow-induced calcium transients, demonstrating that TRPV4, like TRPP2, is an essential component of the ciliary mechanosensor. Because TRPV4-deficient zebrafish and mice lack renal cysts, our findings challenge the concept that defective ciliary flow sensing constitutes the fundamental mechanism of cystogenesis.