Neurons rely on dendrites for the acquisition of sensory and synaptic input from their particular receptive fields. Findings of aberrant dendritic morphology in disorders such as autism spectrum disorder (ASD) and schizophrenia highlight the importance of understanding how complex dendritic arbors are developed and maintained. The goal of this project is to characterize mechanisms of dendritic outgrowth and regulation of field size using the multi-dendritic FLP and PVD mechanosensory neurons of C. elegans as a model. The dendritic arbor of FLP covers the head of the worm while the arbor of PVD covers the body. Here, we provide a detailed characterization of FLP and PVD field size throughout development and demonstrate that field size is regulated at least in part by contact-mediated repulsion. Additionally, using an unbiased forward genetic approach, we isolated a mutant allele,
dz197, in
unc-33/Collapsin Response Mediator Protein (CRMP), which differentially effects FLP and PVD receptive field sizes. Previous studies of UNC-33/CRMP null mutants have shown that it is required for establishing microtubule polarity in PVD by binding microtubules and through interaction with a protein complex, anchoring them to the membrane. However, these functions are specific to the UNC-33 long isoform, and no clear roles have been attributed to the medium and short UNC-33 isoforms. We found that
dz197 mutants display distinct phenotypes from UNC-33 null mutants both in FLP and PVD morphology as well as in locomotion. Unlike null mutants,
dz197 mutants can be rescued by expression of UNC-33S. We hypothesize that differences between phenotypes in
dz197 mutants and UNC-33 null mutants are due to the
dz197 mutation disrupting oligomerization between various UNC-33 isoforms and that oligomerization is required for microtubule binding. Comparisons between
dz197 and null mutants may reveal specific roles for UNC-33 in establishing dendritic field size and may reveal differences in field size regulation between FLP and PVD.