Dendrites establish proper neural networks, allowing normal brain functions such as social networking, learning, and memory. Thus, it is no surprise that dendritic defects are associated with many neurological disorders. Accordingly, understanding the molecular mechanisms behind dendrite formation and maintenance is an important research goal. Recent investigations of dendrite morphogenesis have highlighted the importance of gene regulation at the post-transcriptional level. The CPEB class of RNA-binding proteins mediates many post-transcriptional mechanisms, and homologs of this protein have previously been identified as important in synaptic plasticity and dendrite morphogenesis. Here, we identify the Caenorhabditis elegans CPEB homolog CPB-3 as necessary for typical dendritic branching in the PVD multidendritic sensory neuron. This study also points to a previously undescribed function of a CPEB; loss of CPB-3 causes gene expression profile changes in touch neurons. Thus, we believe that CPB-3 is a very strong candidate for regulating the transport and translation of target mRNAs within dendrites. Furthermore, the CPB-3 homolog CPEB1 is expressed in the human brain suggesting that this RNA-binding protein is a candidate regulator of dendrite development in humans.