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First published online 30 August 2006
doi: 10.1242/dev.02555
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1 Laboratory of Genetics,, Division of Pharmaceutical Sciences, University of
Wisconsin-Madison, Madison, WI 53705-2222, USA.
2 School of Pharmacy, Division of Pharmaceutical Sciences, University of
Wisconsin-Madison, Madison, WI 53705-2222, USA.
3 Department of Molecular, Cellular and Developmental Biology, Yale University,
New Haven, CT 06511, USA.
Author for correspondence (e-mail:
mmbarr{at}pharmacy.wisc.edu)
Accepted 27 July 2006
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.
Key words: Autosomal Dominant Polycystic Kidney Disease, C. elegans, TRPP2 (PKD2)/PKD-2
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