Sensory neurons rely on specialized structures called cilia to transduce environmental stimuli. Olfactory cilia located in the nasal cavity are directly exposed to the external environment and are therefore particularly vulnerable to injury and infection. Disruption of olfactory cilia morphology can lead to anosmia, or loss of the sense of smell. Despite the clear importance of cilia integrity for olfaction, the molecular mechanisms that drive cilia regrowth and restore sensory function are not well understood. To investigate how cilia regenerate following damage, we are utilizing the nematode Caenorhabditis elegans as a genetically tractable model organism. We have developed a genetic mutant background that enables inducible truncation of C. elegans olfactory cilia followed by rapid regrowth. Using this system, we have previously conducted a forward genetic screen to identify mutants with specific disruptions in cilia regrowth and not initial ciliogenesis, using neuronal uptake of a lipophilic dye as a readout. We are now using green fluorescent protein (GFP) to visualize olfactory cilia in targeted neurons, and we are precisely quantifying cilia regrowth to identify the most promising regulators of regeneration. From the highest-priority candidate mutants exhibiting the most robust regrowth defects, we are expanding worm populations and isolating genomic DNA for whole-genome sequencing to identify causal mutations. Given the strong conservation of cilia genes across species, this work has the potential to uncover fundamental and conserved molecular regulators of cilia regeneration that may ultimately inform therapeutic strategies aimed at restoring cilia structure following damage or in diseases associated with ciliary dysfunction.