Student Theses and Dissertations

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RU Laboratory

Bargmann Laboratory


Variation in behavior among individuals is both remarkable and of great significance to society. People differ in locomotor skills, in sleep patterns, in their willingness to take risks, and in how they relate to other people. Whereas diversity enriches society, extreme behavioral deviations can be pathological, so it is important to identify the causes of behavioral variability. It is clear that both the environment and genetics contribute to behavioral diversity in all animals, but the nature of the specific genes involved is only beginning to emerge. The nematode worm Caenorhabditis elegans is a good animal model to study the genetic and neuronal bases of behavioral variation, as there are large differences in behavior between naturally-occurring strains, and powerful tools exist to characterize these differences. One example of the behavioral diversity of C. elegans is the existence of different thresholds for exploration–exploitation tradeoffs: some strains decide to exploit resources more thoroughly, while others decide to abandon resources earlier and explore other options. Using quantitative genetic tools I have found that genetic variation in the adrenergic receptor tyra-3 affects this exploration– exploitation decision. tyra-3 responds to the neurotransmitter tyramine, which is related to vertebrate adrenaline and noradrenaline. tyra-3 modifies the activity of sensory neurons that detect food cues and that regulate the decision to abandon depleting food resources. In strains that are more prone to exploration tyra-3 is expressed at lower levels, and this altered expression modifies the response of the sensory neurons to food. Variation in a gene that affects the response to the environment helps explain how nature and nurture interact to produce behavioral outcomes. In addition to variation in exploratory behavior, C. elegans strains also differ in social behaviors. In most strains animals aggregate with each other, whereas a few strains have evolved a solitary life-style. Variation in the neuropeptide Y receptor homologue npr-1 contributes to social behavior variation, but I found that other genes are also involved in this behavior. Through quantitative genetic analysis I identified polymorphisms in the GABA-gated cation channel exp-1 that generate variation in social behavior. Based on existing behavioral diversity in C. elegans, I discovered genetic variation in two neurotransmitter receptors and characterized the way in which this variation modifies the neuronal circuits that generate behavior. Consistent with findings in other systems, my results suggest that genetic variation in neurotransmitter receptors is a common way of generating behavioral diversity in animals.


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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