Bedoukian   RussellIPM   RussellIPM   Piezoelectric Micro-Sprayer


Home
Animal Taxa
Plant Taxa
Semiochemicals
Floral Compounds
Semiochemical Detail
Semiochemicals & Taxa
Synthesis
Control
Invasive spp.
References

Abstract

Guide

Alphascents
Pherobio
InsectScience
E-Econex
Counterpart-Semiochemicals
Print
Email to a Friend
Kindly Donate for The Pherobase

« Previous AbstractClimate change-induced vegetation change as a driver of increased subarctic biogenic volatile organic compound emissions    Next AbstractCharacterisation of different types of hay by solid-phase micro-extraction-gas chromatography mass spectrometry and multivariate data analysis »

Elife


Title:Impairing one sensory modality enhances another by reconfiguring peptidergic signalling in Caenorhabditis elegans
Author(s):Valperga G; de Bono M;
Address:"Cell Biology Division, MRC Laboratory of Molecular Biology, Cambridge, United Kingdom. Institute of Science and Technology Austria (IST Austria), Klosterneuburg, Austria"
Journal Title:Elife
Year:2022
Volume:20220224
Issue:
Page Number: -
DOI: 10.7554/eLife.68040
ISSN/ISBN:2050-084X (Electronic) 2050-084X (Linking)
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. 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"
Keywords:"Animals Animals, Genetically Modified Caenorhabditis elegans/genetics/*metabolism Caenorhabditis elegans Proteins/genetics/*metabolism Calcium/metabolism GTP-Binding Protein alpha Subunits, Gi-Go/metabolism Genetic Testing/methods Mutation Neuropeptides/m;"
Notes:"MedlineValperga, Giulio de Bono, Mario eng WT_/Wellcome Trust/United Kingdom MC_U105178786/MRC_/Medical Research Council/United Kingdom P40 OD010440/OD/NIH HHS/ 209504/Z/17/Z/WT_/Wellcome Trust/United Kingdom Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't England 2022/02/25 Elife. 2022 Feb 24; 11:e68040. doi: 10.7554/eLife.68040"

 
Back to top
 
Citation: El-Sayed AM 2024. The Pherobase: Database of Pheromones and Semiochemicals. <http://www.pherobase.com>.
© 2003-2024 The Pherobase - Extensive Database of Pheromones and Semiochemicals. Ashraf M. El-Sayed.
Page created on 23-11-2024