Use this URL to cite or link to this record in EThOS: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.596894
Title: Genetics of carbon dioxide avoidance behaviour in Caenorhabditis elegans
Author: Bretscher, A. J.
Awarding Body: University of Cambridge
Current Institution: University of Cambridge
Date of Award: 2009
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Abstract:
I examine the CO2 response of the nematode C. elegans. This species inhabits rotting material, which typically has a broad CO2 concentration range. I show that well-fed C. elegans avoid CO2 levels greater than 0.5%. Animals can respond to changes in CO2 levels in seconds. Responses to CO2 do not reflect avoidance of acid pH but appear to define a new sensory response. Sensation of CO2 is promoted by the cGMP-gated ion channel subunits TAX-2 and TAX-4. TRPV (transient receptor potential vanilloid-type) channels appear to play only a minor role in CO2 avoidance. The transmembrane guanylate cyclase daf-11 is required to promote CO2 avoidance off food, but not on food. CO2 avoidance is promoted by DAF-11 activity in the AWB neurons, which express tax-2 and tax-4. Starvation strongly suppresses CO2 avoidance. Robust CO2 avoidance in well-fed animals requires inhibition of the DAF-16 forkhead transcription factor by the insulin-like receptor DAF-2. Although starvation activates DAF-16, daf-16 alone is not responsible for starvation-induced suppression of CO2 avoidance. Interestingly, exposure to hypoxia (<1% O2) also suppresses CO2 avoidance, via activation of the hypoxia inducible transcription factor, HIF-1. The npr-1 215V allele of the naturally polymorphic neuropeptide receptor npr-1, besides inhibiting avoidance of high O2 in feeding C. elegans, also promotes avoidance of high CO2. NPR-1 215V acts in the ASE neurons to promote CO2 avoidance. C. elegans integrates competing CO2 and O2 sensory inputs such that either the CO2 or the O2 response dominates. Food and allelic variation at NPR-1 determine which response dominates. To identify C. elegans CO2 receptors, I performed an EMS mutagenesis screen for carbon dioxide avoidance defective (Cdad) mutants. One Cdad isolate, db130, revealed a novel H377E missense mutation in the C. elegans Protein Kinase B orthologue, akt-1.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.596894  DOI: Not available
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