Caenorhabditis elegans
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA94241 | ENA |
REPOSITORIES: ENA
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Project description: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.
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Project description:These experiments were undertaken with the goal of identifying genes whose expression is enriched in or restricted to the sensory rays of the C. elegans male tail. We constructed two mutant strains in which ray development is either compromised (EM672) or enhanced (EM673), and harvested mRNA from adult males. Labeled cDNAs were compared on seven arrays (representing three different sets of mRNA preps). In all experiments, Channel 1 (green) represents the EM672 expression profile and Channel 2 (Red) corresponds to EM673. Ray-enriched genes would therefore generally be expected to have higher intensities in Channel 2 than in Channel 1. Experimental details and results from these studies are available in D.S. Portman and S.W. Emmons (2004) Identification of C. elegans sensory ray genes using whole-genome expression profiling. Groups of assays that are related as part of a time series. Computed
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