Neural cells are characterized by their diverse, often highly elaborate, cellular morphologies. The structural diversity within the nervous system provides the functional versatility necessary for the emergence of complex behaviors. Defects in neuronal morphology are associated with neurological disorders; therefore, understanding the molecular mechanisms that establish neuronal architecture has important implications for human health and disease. The Caenorhabditis elegans multidendritic sensory PVD neurons, which structurally resemble mammalian polymodal nociceptors, are a popular model for studying neuronal morphogenesis in vivo. Based on recent studies, post-transcriptional regulation of gene expression, including alternative pre-mRNA splicing, has emerged as an important means of control during neuronal morphogenesis. A suite of functionally conserved RNA-binding proteins with post-transcriptional roles in Drosophila melanogaster and C. elegans sensory neuron dendrite patterning have since been identified. Among these proteins are the Muscleblind splicing factors MBL/MBL-1, which have human homologs MBNL1-3 that are associated with myotonic dystrophy. Here we show that loss of C. elegans mbl-1 function produces an aberrant PVD sensory neuron dendritic arbor, characterized by reduced dendrite terminal branching that becomes more severe with increasing distance from the neuronal cell body. We tested whether similar defects would be apparent for other types of C. elegans sensory neurons and confirmed the previous findings that the P/ALM and P/AVM gentle touch receptors exhibit truncated axons, and that the PLM synapse is positioned abnormally close to the cell body. We add the finding that the PLM dendrite is elongated in the mbl-1 mutant. To test whether mbl-1 function is required within muscle or within the nervous system to regulate PVD terminal dendrite patterning, we co-expressed muscle and PVD reporters within the same transgenic line to observe the muscle/PVD interface. We show that, beyond the reduction in terminal branches, loss of mbl-1 function does not affect the stereotyped patterning of PVD muscle-skin interface innervation, and no defects in the macrostructure of the body wall muscle were evident in the mutant. Work from other labs has shown that mbl-1 mutants fail to localize pre-synaptic proteins in the distal axon while excluding these components from the dendrite in some neuron types. Ongoing work in the lab seeks to test whether the PVD neuron displays a similar synaptic protein trafficking defect by expressing mCherry-tagged RAB-3 in the PVD neuron and monitoring its subcellular localization. Previous findings indicate that mbl-1 might regulate PLM axon outgrowth by influencing the stability of mec-7 (β-tubulin) and mec-12 (α-tubulin) mRNA. We are testing whether decreased MEC-7 expression upon loss of mbl-1 function might contribute to the dendrite patterning defect observed in the PVD neuron by overexpressing mec-7 using a PVD-specific promoter. MBL-1 is predicted to function as a regulator of alternative splicing; to learn more about how defects in splicing may lead to neuron morphological changes, we aim to identify the direct mRNA targets of MBL-1 binding/regulation using ribonucleoprotein (RNP) immunoprecipitation followed by RNA sequencing. The identity and function of these targets may offer insights into the post-transcriptional mechanisms that regulate neuron morphogenesis.