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

Abstract

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.

Figure 1. dmd-10 mutant worms display the typical number of amphid sensory neurons pairs

(A) Map of the positions of C. elegans ASH, ADL, ASI, AWB, ASK, and ASJ sensory neurons. (B-D) DiI labeled ASH, ASI, ADL, ASK, AWB, and ASJ sensory neurons of a representative wildtype (WT)(B) cam-1 (C) and dmd-10 (D) wormvisualized via fluorescence microscopy. Images show the presence of each fluorescently-labeled sensory neuron cell body (white solid arrows) in both the left (L) and right (R) sets. Yellow arrowheads note missing ASI cell bodies in cam-1 worms. (E) Graphs show the proportion worms with DiI filled amphid neurons for each genotype (WT n=34, cam-1 n=36, dmd-10 n=31). Unfilled portion of each bar represents proportion of worms with 1 out of 2 neurons observed. *=p<0.05 Chi-squared test, cam-1 compared to wildtype.