Individual C. elegans neurons display differential sensitivity to smn- 1 silencing.

Spinal muscular atrophy is a neuromuscular disorder primarily caused by mutations in the SMN1 (Survival of Motor Neuron 1) gene. SMN1 is ubiquitously expressed and encodes a protein essential for the assembly of small nuclear ribonucleoproteins, key components of pre-mRNA splicing. The SMN protein also participates in several other fundamental cellular processes, including RNA transport, regulation of actin dynamics, transcription, and translation. While multiple hypotheses have been put forward to explain the selective motor neurons (MNs) vulnerability to SMN deficiency, the precise mechanisms involved remain incompletely understood. In this study, we used neuron-specific smn-1 RNAi silencing in D-type MNs or in touch receptor neurons in C. elegans In touch receptor neurons, smn-1 silencing caused distinct defects in neuronal process morphology. Our results reveal pronounced neuron-specific differences in sensitivity within the neurons of C. elegans, providing a robust framework to dissect the mechanisms underlying selective neuronal vulnerability of spinal cord MNs in spinal muscular atrophy.