EducationB.A., University of Colorado, Boulder, 1990
Ph.D., University of California, Berkeley, 2000
There is a postdoctoral position available in Dr. Eaton's lab. Click for details.
We hope to understand the molecular mechanisms underlying the highly specified formation and elimination of synaptic connections. The remodeling of synaptic contacts is critical for the formation of neural circuitry during development and represents the basis of learning and memory in the adult. Importantly, the inappropriate loss of synaptic contacts is a hallmark of many neurodegenerative diseases suggesting a possible link between mechanisms normally involved in synaptic remodeling and neurodegenerative disease. The Eaton lab uses genetic, cellular, and functional analyses to identify and characterize genes required for the growth and stabilization of synaptic contacts using the Drosophila model system.
We are currently using forward genetic approaches to identify genes and processes required for the growth and stabilization of synapses. Importantly, one of the initial genes found to be required for synaptic growth and stability, glued, has been genetically linked to lower motor disease supporting a molecular link between the regulation of synaptic connectivity and neurodegenerative disease.
1) Synaptic proteasome regulation: A large-scale screen has implicated the regulation of synaptic protein degradation as an important role for the dynactin complex within the nervous system. We are combining molecular genetic techniques with in vivo cellular analyses to investigate the role of the dynactin complex in the process of synaptic protein degradation, especially the regulation of synaptic proteasome function. Changes in synaptic proteasome activity have been associated with both synaptic strengthening and synaptic elimination, but how synaptic proteasome function is regulated is unclear.
2) Effects of aging on synaptic function: In combination with genetic approaches, we are using the onset and the progression of synaptic dysfunction as assays to identify the cellular processes that determine the pathogenesis of late onset neurological disease. These studies aim to elucidate the molecular targets of aging within the synapse and determine how these alterations contribute to neurodegeneration. It is expected that these studies will identify novel mechanisms that underlie the loss of synaptic function observed with age.