GSE168597
Impairing one sensory modality enhances another by reprogramming peptidergic circuits in Caenorhabditis elegans.
Abstract: Animals that lose one sensory modality often show augmented responses to other sensory inputs. The mechanisms underpinning this cross-modal plasticity are poorly understood. To probe these mechanisms, we perform a forward genetic screen for mutants with enhanced O2 perception in C. elegans. Multiple mutants exhibiting increased responsiveness to O2 concomitantly show defects in other sensory responses. One mutant, qui-1, defective in a conserved NACHT/WD40 protein, abolishes pheromone-evoked Ca2+ responses in the ADL chemosensory neurons. We find that ADL's responsiveness to pre-synaptic input from O2-sensing neurons is heightened in qui-1 and other sensory defective mutants resulting in an enhanced neurosecretion. Expressing qui-1 selectively in ADL rescues both the qui-1 ADL neurosecretory phenotype and enhanced escape from 21% O2. Profiling of ADL neurons indicates its acquired O2-evoked neurosecretion is the result of a transcriptional reprogramming that up-regulates neuropeptide signalling. We show that the conserved neuropeptide receptor NPR-22 is necessary and sufficient in ADL to enhance its neurosecretion levels. Sensory loss can thus confer cross-modal plasticity by re-wiring peptidergic circuits. Overall design: In this dataset we compare the transcriptome of ADL sensory neurons between wild types and qui-1 mutants. To isolate ADL sensory neurons we dissociate animals where ADL neurons are markered by a fluorescent protein (mKate2) expressed under the control of an ADL-specific promoter (srh-220p). Sample size: N= 6 (WT), N=4 (qui-1).