General and cell-type specific mechanisms target TRPP2/PKD-2 to cilia

Young Kyung Bae, Hongmin Qin, Karla M. Knobel, Jinghua Hu, Joel L. Rosenbaum, Maureen M. Barr

Research output: Contribution to journalArticlepeer-review

75 Scopus citations


Ciliary localization of the transient receptor potential polycystin 2 channel (TRPP2/PKD-2) is evolutionarily conserved, but how TRPP2 is targeted to cilia is not known. In this study, we characterize the motility and localization of PKD-2, a TRPP2 homolog, in C. elegans sensory neurons. We demonstrate that GFP-tagged PKD-2 moves bidirectionally in the dendritic compartment. Furthermore, we show a requirement for different molecules in regulating the ciliary localization of PKD-2. PKD-2 is directed to moving dendritic particles by the UNC-101/adaptor protein 1 (AP-1) complex. When expressed in non-native neurons, PKD-2 remains in cell bodies and is not observed in dendrites or cilia, indicating that cell-type specific factors are required for directing PKD-2 to the dendrite. PKD-2 stabilization in cilia and cell bodies requires LOV-1, a functional partner and a TRPP1 homolog. In lov-1 mutants, PKD-2 is greatly reduced in cilia and forms abnormal aggregates in neuronal cell bodies. Intraflagellar transport (IFT) is not essential for PKD-2 dendritic motility or access to the cilium, but may regulate PKD-2 ciliary abundance. We propose that both general and cell-type-specific factors govern TRPP2/PKD-2 subcellular distribution by forming at least two steps involving somatodendritic and ciliary sorting decisions.

Original languageEnglish (US)
Pages (from-to)3859-3870
Number of pages12
Issue number19
StatePublished - Oct 2006


  • Autosomal dominant polycystic kidney disease
  • C. elegans
  • TRPP2 (PKD2)/PKD-2

ASJC Scopus subject areas

  • Molecular Biology
  • Developmental Biology


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