Student Theses and Dissertations

Date of Award


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RU Laboratory

Bargmann Laboratory


social behavior, C. elegans, deathmone, social feeding


Most animal species, from simple invertebrates to complex mammals, require behavioral mechanisms to communicate with and respond to conspecifics, whether to mate, to assess predatory danger, or evaluate the nutritional quality of the surrounding environment. Understanding the molecular and cellular underpinnings of these social behaviors remains a central challenge in neurobiology. I used the nematode C. elegans as a model system to study the genetics and neural circuitry that underlie social behavior. First, I evaluated the behavioral responses of C. elegans to a nematode extract (deathmone), which served as a model for alarm pheromones in other animal species (chapter 2). Worms showed acute avoidance of deathmone, and reduced their exploration when cultivated on it, a behavior termed “dwelling.” I combined chemical analysis, laser ablation studies, and genetic studies to identify the sensory neurons and molecular signaling pathways that promote dwelling in response to deathmone. Second, I investigated the neuronal substrates responsible for social feeding, a behavior in which certain strains of C. elegans display high lomocotory speeds, accumulate on the border of bacterial food lawns, and aggregate into groups. A low activity or null allele of the neuropeptide y receptor homologue npr-1 promotes social feeding, while a high activity form—which is found in the wild-type N2 strain—promotes solitary behavior1. Expression of a high-activity npr-1 cDNA specifically in the interneuron RMG converted npr-1 loss-of-function mutants from social feeders into solitary ones. The RMG neurons are gap junctional hubs that electrically couple the sensory neurons URX, ASH, and ADL—all previously implicated in social feeding—and the pheromone-sensing neuron ASK, suggesting that social feeding and pheromone responses may be related. Indeed, npr-1 social feeders are attracted to ascarosides, while N2 solitary feeders are repelled, a behavioral difference that is dependent on RMG function. Calcium imaging of ASK and its postsynaptic partner AIA demonstrated that RMG promotes signaling from ASK to AIA. Taken together, these data provide a common neural circuitry for social behaviors in C. elegans, and offer some insights into the molecular mechanisms of their regulation.


A thesis presented to the faculty of The Rockefeller University in partial fulfillment of the requirements for the degree of Doctor of Philosophy.

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