AbstractCiliary 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.