Mechanical stimuli on the skin of C. elegans are detected by the dendritic arbors of PVD nociceptive neurons, which provide uniform sensory coverage outside the head region across the entire animal. Through genetic screens, we isolate three mutants that display profound dendrite branching and self-avoidance defects in PVD neurons and through whole genome sequencing, we identify the responsible mutations in the
kpc-1 gene. Compared to wild-type animals, a strong
kpc-1 mutant allele exhibits a significantly lower number of secondary dendrite branches whereas a weak
kpc-1 mutant allele displays tertiary dendrite self-avoidance defects. Although
kpc-1 was previously implicated in dendrite branching and self-avoidance, the mechanism by which
kpc-1 regulates the process is unknown. Here, we show that the
kpc-1 3' UTR is required for the
kpc-1's function in dendrite branching and self-avoidance. The
kpc-1 3'UTR facilitates
kpc-1 RNA localization to branching points and contact points between sibling dendrites. Using fluorescence recovery after photoconversion, we show that the
kpc-1 3'UTR promotes local translation in the distal segment of PVD dendrites. We identify an important secondary structural motif in the
kpc-1 3'UTR required for tertiary dendrite self-avoidance. We demonstrate that over-expression of
kpc-1 leads to greater self-avoidance without limiting initial dendrite outgrowth, supporting a direct role of
kpc-1 in self-avoidance. Animals with
dma-1 receptor over-expression display similar secondary dendrite branching and tertiary dendrite self-avoidance defects that are suppressed with
kpc-1 over-expression, which suggests that DMA-1 is a potential KPC-1 target that is down-regulated by KPC-1. Our results support a model where KPC-1 is expressed at the branching points and the contact points between neighboring dendrites to locally down-regulate DMA-1 receptors to promote dendrite branching and self-avoidance.