| Popis: |
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 O2perception inC. elegans. Multiple mutants exhibiting increased responsiveness to O2concomitantly 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 inqui-1and other sensory defective mutants resulting in an enhanced neurosecretion. Expressingqui-1selectively in ADL rescues both thequi-1ADL 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. |
