Neurons exhibit distinct morphological domains, axons and dendrites, which are essential for functional wiring of the nervous system. While many molecules involved in axon development have been discovered, there is little known about the molecules and mechanisms required for dendrite formation. To understand how dendrites develop in C. elegans we have chosen to study the oxygen sensory neuron, PQR. The PQR neuron has its cell body positioned in the left lumbar ganglion on the posterior-lateral body. From the cell body two processes extend. A single dendrite extends posteriorly towards the tail ending with a cilium in the pseudocoelom. On the opposite side, an axon extends anteriorly joining the ventral nerve cord and terminating in the midbody region. PQR is born post-embryonically during the L1 stage, allowing easy visualization of dendrite and axon development using the gcy-36::GFP transgene. We have used a candidate-mutant approach to identify genes involved in dendrite formation. The secreted Wnt ligand, LIN-44, regulates neuronal polarity in PLM mechanosenosory neurons in the C. elegans tail. We found that LIN-44 specifically regulates dendrite formation in PQR. In lin-44 mutants, the PQR dendrite was often shortened or absent. This defect appeared in the initial stages of development (at the L1 stage) and persisted until adulthood, suggesting that the phenotype results from a failure in dendrite development rather than the presence of ectopic pruning. Interestingly, the PQR axon was not affected in these animals, indicating a dendrite-specific effect of LIN-44 on this cell. LIN-44 is expressed by hypodermal cells in the tip of the tail, a position that is posterior to the PQR cell body. The PQR dendrite develops towards the region where LIN-44 is expressed, and thus this ligand may act as an attractant cue for the growing dendrite. LIN-17/Frizzled acts as a receptor for LIN-44 in regulating neuronal polarity and other biological processes. We found that lin-17 mutant animals presented defects in PQR dendrite development similar to those observed in lin-44 mutants: PQR dendrite was shortened or absent, while the axon was unaffected. Thus, as for lin-44, the lin-17 gene has a dendrite specific effect. Our results suggest that Wnt molecules and Frizzled receptors are key molecules required for PQR dendrite formation.