Neurological disorders often present with defects in dendritic arborization, illustrating the significance of dendrites and synaptic connections for cognition. As such, it is important to the study of these disorders to understand the mechanism by which neurons establish proper dendritic morphology. Because dendrites are distantly located from the nucleus and exhibit independent changes in growth and connectivity, regulation of dendrite morphogenesis likely occurs through a localized post-transcriptional mechanism. RNA-binding proteins are important mediators of post-transcriptional regulation and several such proteins have been implicated in dendrite development. The RNA-binding protein, Nanos, has been previously characterized as important for dendrite morphogenesis in Drosophila. However, knockout of nos-1, the strongest nanos homolog in C. elegans, does not reveal significant dendrite defects. Due to the presence of two additional nos paralogs in the C. elegans genome, nos-2 and nos-3, we suspected that the lack of dendrite defects upon knockout of nos-1 indicated the possibility of genetic redundancy. Our results support the notion that the nos paralogs are genetically redundant and further identifies the redundant function of these proteins as important for fourth order dendrite morphogenesis in C. elegans. Furthermore, this study also identifies nos-3 alone as important for the morphogenesis of second and third order dendrites. The expression pattern of the three NOS proteins in the C. elegans PVD neuron is also consistent with the predicted function of NOS as a translational regulator, suggesting a role for the nos paralogs in dendrite development and maintenance.