| Although at times simple in its manifestations, animal behavior is dictated by an enormous network of cellular and molecular interactions. Attempts to identify the biological bases of behavior in mammalian systems must inevitably deal with the complexity of these nervous systems. In contrast, the nematode C. elegans has 302 neurons whose characterization established a unique system to dissect out the cellular and molecular substituents of various behaviors. With so few neurons to mediate all aspects of its neurobiology, understanding how a particular cell functions in the context of its neighbors and the genes that comprise those functions promises great yield. In this thesis, I will focus on one particular interneuron class, AIY, and the integral role it plays in modifying locomotory behavior by linking pre-synaptic sensory neurons to downstream motor output. Specifically, AIY is positioned downstream of a number of different sensory neuron types including thermosensors, odorsensors and chemosensors. These different sensory inputs can be either attractive or repulsive and as such, the behavioral responses to these stimuli will vary. The nature of the behavioral response is encoded within the sensory neuron or in its signaling to the downstream AIY interneuron. AIY then signals through several additional interneurons to ultimately affect the activity of the command interneurons, responsible for generating forward and backward movement in the worm. This network can be modified by changes in the environment and acts in parallel to other similar neuronal networks. Having characterized the role of AIY in this behavioral response, I next sought to identify the molecular mediators of this function. Mutations exist in a number of genes known to be expressed in AIY. I will present a behavioral characterization of these various mutants with respect to the known roles of AIY. Whereas mutations affecting early-acting transcription factors in AIY such as ttx-3 abrogate AIY activity, none of the downstream genes analyzed phenocopy loss of AIY activity. |
