Many of the behaviours of C. elegans are mediated by the worm's ability to orient itself towards chemical gradients or other sensory cues. Two mechanisms of orientation have been observed in the worm: pirouettes and steering. Past studies have identified a number of neuron classes that contribute to navigation by linking neuronal laser ablations and observations of mutants to changes in body postures and locomotion statistics1,2. Recently, optogenetic manipulation has also shed light on the neuronal control of the worm's chemotactic behaviour3. SMB motor neurons have been postulated to be part of the navigation circuit. We have generated a chromosomally-integrated transgenic line (UL4230) where the SMBs are genetically ablated in early larvae. The line demonstrates a loopy phenotype similar to that previously observed following laser-ablation of SMBs1. We have also targeted another class of neuron, located close to and highly connected via synapses to the SMBs but not previously explored: the SAA interneurons. We initially used expression of GFP to confirm that the selected promoters drove expression in the location originally described. A combination of
lad-2 and
unc-42 promoters was used to genetically ablate the SAAs by targeted expression of the worm's caspase, as encoded by two distinct parts of the
ced-3 gene, such that the intact enzyme is produced only in these neurons specifically4. Absence of GFP expression confirmed the specific and targeted ablation of the SAAs. The generated strains, with SMBs or SAAs ablated (UL4230 and UL4207), demonstrated a phenotype different to that of N2 in both spontaneous and evoked locomotion. Locomotion was evoked using a radial gradient of NH4Cl. Initial results suggest that both SMBs and SAAs suppress the probability of pirouettes and decrease the amplitude of sinusoidal undulations. Additional experiments are underway to explore the contributions of SAA and SMB, separately and together, to undulations and steering, and to link those to the pirouette initiation pathway. 1. Gray J. M., et al., (2005). A circuit for navigation in Caenorhabditis elegans. Proc. Natl. Acad. Sci. U.S.A, 102(9). 2. Iino Y., and Yoshida K. (2009). Parallel use of two behavioral mechanisms for chemotaxis in Caenorhabditis elegans. Journal of Neuroscience, 29(17). 3. Kocabas A., et al., (2012). Controlling interneuron activity in Caenorhabditis elegans to evoke chemotactic behaviour. Nature, 490(7419). 4. Chelur D. S., and Chalfie M. (2007). Targeted cell killing by reconstituted caspases. Proc. Natl. Acad. Sci., 104(7).