DMD-10 is dispensable for the initial development of amphid sensory neurons and their survival in mature C. elegans.

Mechanosensory or chemosensory activation of glutamatergicASH amphid sensory neurons promotes avoidancebehaviors in C. elegans. Wormswith mutations in the transcription factor DMD-10 have impaired ASH-mediated sensorimotor reflexes. We hypothesized that the behavioral dysfunction in dmd-10 mutants could arise from impaired ASH development or survival leading to disrupted glutamatergic signaling.To test this, we performed in vivo fluorescence microscopy of young adult C. elegans amphid neurons after labeling with the lipophilic dye DiI. We quantified the number of ASH neurons as well as five other amphid sensory neuron pairs. We found that the number of amphid neurons in dmd-10 mutants was the same as in wild-type worms. Our results suggest that dmd-10 is not required for amphid neuron development or survival in mature C. elegans.