Neurons are polarized cells with specialized processes known as dendrites that receive environmental stimuli and transduce that input to the cell body, or soma. Dendrites are important in generating action potentials for cell-to-cell communication and, in the case of sensory neurons, for sensing the environment. Despite the important role that dendrites play, the molecular mechanisms that regulate dendrite development, or morphogenesis, are poorly understood. Recent research indicates that dendrite morphogenesis is regulated by the localized control of messenger RNA (mRNA) in dendrites. mRNA localization and translational regulation is often mediated by RNA-binding proteins (RBPs), which recognize and bind to specific mRNAs. It is thought that regulating protein translation in dendrites, which are located far from the nucleus where mRNAs originate, is a faster and more efficient way to regulate dendrite morphogenesis than changing gene expression. A recent study has found that the RBP gene brat regulates dendrite morphogenesis in Drosophila. To determine if brat function is conserved, we studied the role of ncl-1, a C. elegans homolog of brat, in dendrite morphogenesis. Dendrite morphology in wild type and ncl-1 mutants was compared using a fluorescent marker that is expressed in the PVD mechanosensory neurons in C. elegans. We find that ncl-1 null mutant PVDs have fewer dendritic branches than wild type throughout development. Consistent with a role in PVD dendritic development, we find that ncl-1 is expressed in most neurons during development, likely including the PVD. Since NCL-1 may be involved in regulating mRNAs in dendrites we wanted to see where within neurons the NCL-1 protein is localized. We find that NCL-1 is localized to both axons and dendrites, but was excluded from the nucleus. Together, these results suggest that NCL-1 plays a conserved role as an RBP that regulates mRNAs important for dendrite elaboration and future studies will be aimed at learning which mRNAs NCL-1 binds and how it regulates them.