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Animals that lose one sensory modality often show augmented responses to other sensory inputs. The mechanisms underpinning this cross-modal plasticity are poorly understood. We probe such mechanisms by performing a forward genetic screen for mutants with enhanced O 2  perception in  Caenorhabditis elegans . Multiple mutants exhibiting increased O 2  responsiveness concomitantly show defects in other sensory responses. One mutant,  qui-1 , defective in a conserved NACHT/WD40 protein, abolishes pheromone-evoked Ca 2+  responses in the ADL pheromone-sensing neurons. At the same time, ADL responsiveness to pre-synaptic input from O 2 -sensing neurons is heightened in  qui-1 , and other sensory defective mutants, resulting in enhanced neurosecretion although not increased Ca 2+  responses. Expressing  qui-1  selectively in ADL rescues both the  qui-1  ADL neurosecretory phenotype and enhanced escape from 21% O 2 . Profiling ADL neurons in  qui-1  mutants highlights extensive changes in gene expression, notably of many neuropeptide receptors. We show that elevated ADL expression of the conserved neuropeptide receptor NPR-22 is necessary for enhanced ADL neurosecretion in  qui-1  mutants, and is sufficient to confer increased ADL neurosecretion in control animals. Sensory loss can thus confer cross-modal plasticity by changing the peptidergic connectome.

Impairing one sensory modality enhances another by reconfiguring peptidergic signalling in Caenorhabditis elegans