Young-Kyung Bae and Jamie Lyman-Gingerich contributed equally to this work.
Special Issue Research Article
Identification of genes involved in the ciliary trafficking of C. elegans PKD-2
Article first published online: 13 APR 2008
Copyright © 2008 Wiley-Liss, Inc.
Special Issue: Special Focus on the Primary Cilium
Volume 237, Issue 8, pages 2021–2029, August 2008
How to Cite
Bae, Y.-K., Lyman-Gingerich, J., Barr, M. M. and Knobel, K. M. (2008), Identification of genes involved in the ciliary trafficking of C. elegans PKD-2. Dev. Dyn., 237: 2021–2029. doi: 10.1002/dvdy.21531
- Issue published online: 23 JUL 2008
- Article first published online: 13 APR 2008
- Manuscript Accepted: 28 FEB 2008
- PKD Foundation
- American Heart Association
- Caenorhabditis elegans;
- sensory neuron;
- transient receptor potential (TRP) channel
Ciliary membrane proteins are important extracellular sensors, and defects in their localization may have profound developmental and physiological consequences. To determine how sensory receptors localize to cilia, we performed a forward genetic screen and identified 11 mutants with defects in the ciliary localization (cil) of C. elegans PKD-2, a transient receptor potential polycystin (TRPP) channel. Class A cil mutants exhibit defects in PKD-2::GFP somatodendritic localization while Class B cil mutants abnormally accumulate PKD-2::GFP in cilia. Further characterization reveals that some genes mutated in cil mutants act in a tissue-specific manner while others are likely to play more general roles in such processes as intraflagellar transport (IFT). To this end, we identified a Class B mutation that disrupts the function of the cytoplasmic dynein light intermediate chain gene xbx-1. Identification of the remaining mutations will reveal novel molecular pathways required for ciliary receptor localization and provide further insight into mechanisms of ciliary signaling. Developmental Dynamics 237:2021–2029, 2008. © 2008 Wiley-Liss, Inc.