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TRPP2 and TRPV4 form a polymodal sensory channel complex

Michael Köttgen1, Björn Buchholz, Miguel A Garcia-Gonzalez

  • 1Renal Division, University Hospital Freiburg, 79106 Freiburg, Germany.

The Journal of Cell Biology
|August 13, 2008
PubMed

Insights

The primary cilium

Area of Science:

  • Cell Biology
  • Biophysics
  • Physiology

Background:

  • Primary cilia are crucial cellular sensors for mechanical stimuli.
  • The molecular basis of ciliary mechanotransduction, particularly calcium signaling, remains unclear.
  • Polycystin-2 (TRPP2) is implicated in ciliary calcium transients but is not mechanosensitive itself.

Purpose of the Study:

  • To elucidate the molecular mechanisms underlying ciliary mechanotransduction.
  • To identify the components of the ciliary mechanosensor responsible for calcium signaling.
  • To investigate the role of TRPV4 in TRPP2-mediated ciliary mechanosensing.

Main Methods:

  • Utilized renal epithelial cells with TRPV4 depletion.
  • Assessed flow-induced intracellular calcium transients.
  • Examined TRPV4-deficient zebrafish and mouse models for renal cyst development.

Main Results:

  • TRPV4 forms a mechano- and thermosensitive complex with TRPP2 within the primary cilium.
  • Depletion of TRPV4 eliminated flow-induced calcium transients in renal epithelial cells.
  • TRPV4-deficient zebrafish and mice did not develop renal cysts.

Conclusions:

  • TRPV4 is an essential component of the ciliary mechanosensor, working with TRPP2.
  • The findings challenge the established model that defective ciliary flow sensing is the primary driver of polycystic kidney disease pathogenesis.

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