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Neural and molecular mechanisms of sensory signal integration in Caenorhabditis elegans

<p> Life exists in complex environments, requiring organisms to have adaptive developmental strategies in order to survive. The nematode <i>Caenorhabditis elegans</i> has evolved a developmental polyphenism whereby it may arrest development in the dauer diapause state when environmental conditions are not suitable for reproductive growth. The relative simplicity of the <i>C. elegans</i> nervous system, together with its robust molecular and genetic tool set, make it an ideal system in which to study how environmental stimuli are sensed and integrated to drive developmental plasticity. Food availability, temperature and the presence of dauer pheromone each inform the dauer fate decision. I have taken molecular and genetic approaches to study the mechanism by which pheromone signals are transduced by <i> C. elegans</i> sensory neurons and also to understand how food and pheromone signals are integrated to drive an adaptive developmental choice. I have identified roles in dauer formation for the protein scaffold QUI-1, the rough endoplasmic reticulum protein MACO-1 and a putative Tau tubulin kinase, which we have named PHD-1. I have also identified a critical role for the calcium/calmodulin-dependent protein kinase 1 CMK-1 in encoding the food signal and integrating this information in the dauer fate decision. Furthermore, these studies have led to the previously unrecognized roles for the ASH and AWC neurons in the regulation of dauer formation.</p>

Identiferoai:union.ndltd.org:PROQUEST/oai:pqdtoai.proquest.com:3703346
Date13 June 2015
CreatorsNeal, Scott Jeffrey
PublisherBrandeis University
Source SetsProQuest.com
LanguageEnglish
Detected LanguageEnglish
Typethesis

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