Life exists in complex environments, requiring organisms to have adaptive developmental strategies in order to survive. The nematode Caenorhabditis elegans 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 C. elegans 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 C. elegans 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.
|Commitee:||Griffith, Leslie C., Haber, James E., Zhang, Yun|
|Department:||Molecular and Cell Biology|
|School Location:||United States -- Massachusetts|
|Source:||DAI-B 76/09(E), Dissertation Abstracts International|
|Subjects:||Molecular biology, Neurosciences, Genetics|
|Keywords:||C. elegans, Camk1, Dauer, Endocrine, Pheromone, Polyphenism|
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