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Impairing one sensory modality enhances another by reprogramming peptidergic circuits in Caenorhabditis elegans.

ABSTRACT: Impairing one sensory modality enhances another by reprogramming peptidergic circuits in Caenorhabditis elegans.

PROVIDER: PRJNA708351 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13919957_1.fastq.gz	Fastqsanger.gz
	SRR13919957_2.fastq.gz	Fastqsanger.gz
	SRR13919958_1.fastq.gz	Fastqsanger.gz
	SRR13919958_2.fastq.gz	Fastqsanger.gz
	SRR13919959_1.fastq.gz	Fastqsanger.gz

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Impairing one sensory modality enhances another by reprogramming peptidergic circuits in Caenorhabditis elegans.

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

Project description: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 O2 perception in Caenorhabditis elegans. Multiple mutants exhibiting increased O2 responsiveness 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 pheromone-sensing neurons. At the same time, ADL responsiveness to pre-synaptic input from O2-sensing neurons is heightened in qui-1, and other sensory defective mutants, resulting in enhanced neurosecretion although not increased Ca2+ responses. Expressing qui-1 selectively in ADL rescues both the qui-1 ADL neurosecretory phenotype and enhanced escape from 21% O2. 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.

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