Cytoskeletal microtubules support many critical cellular processes including mitosis, organelle transport and support for cellular extensions. Because the C. elegans genome encodes nine alpha-tubulin and six beta-tubulin isoforms, the largely conserved structure among paralogous tubulins raises the question of functional specialization. Are all tubulins equivalent, or do they have unique roles in specific cellular and developmental contexts? We have addressed this question by analyzing axonemal tubulins. Using data from recent genomic approaches, we identified two alpha-tubulins,
tba-6 and
tba-9, and one beta-tubulin,
tbb-4, as likely components of the microtubule cytoskeleton in ciliated C. elegans neurons. Using transcriptional and translational reporter genes, we have found that these tubulins are expressed in specific subsets of sensory neurons in both sexes, localizing to the ciliated endings of dendrites. Because combinations of these tubulins are expressed in ciliated ray sensory neurons in the male tail, we assessed ray neuron function in males lacking
tba-6,
tbb-4, and/or
tba-9. All single, pairwise double, and triple mutant animals were defective in the response to hermaphrodite contact, indicating that specific tubulins are necessary for optimal sensory function. We have also found that certain tubulins are important for other functions, consistent with their expression in a variety of sensory neurons. For example, single
tba-9 mutant animals exhibited abnormalities in many parameters of locomotion and increased foraging, while triple mutants exhibited reduced exploratory behavior compared to wild type in dwelling assays. We have also examined the localization of signaling molecules, the structure of cilia, and components of intraflagellar transport (IFT) in order to better understand the roles of specific tubulins in sensory neurons. We observed that PKD-2, a TRP channel expressed in ray neurons, is mislocalized in mutants lacking
tba-6 or
tbb-4. However, preliminary data indicate that the localization of the IFT component OSM-6 does not appear to be disrupted in these single mutants. In addition, we examined the structure of the distal dendrite and cilia in the CEM neurons with KLP-6::GFP, a kinesin family member. We observed gross abnormalities in single
tba-6 mutants that are enhanced by mutations in
tbb-4. We are in the process of using additional markers to further analyze axoneme and transition zone structure. Together, our studies support a model in which specific tubulins build specialized axonemes that optimize sensory function.