Our Research
We use genetic and molecular approaches in the small nematode C. elegans to understand the conserved mechanisms underlying neurodegenerative disease and nervous system function. We focus on delineating cellular and molecular pathways pertinent to Huntington's disease, Spinal Muscular Atrophy, Amyotrophic Lateral Sclerosis, Frontotemporal Dementia, Alternating Hemiplegia of Childhood, and other neurodegenerative diseases. We also study the genetic and molecular mechanisms regulating sleep and fatigue.
Our laboratory undertakes behavioral, molecular, and genetic studies to understand the conserved mechanisms underlying behavior. Past work focused on how animals respond to changes in the environment. This resulted in the identification of a new family of conserved Notch co-ligands in C. elegans that play diverse roles regulating stress response. Current research examines the conserved molecular pathways that regulate sleep and fatigue.
We use forward and reverse genetic techniques to identify pathways critical for neurodegenerative disease and have established the utility of C. elegans for modeling these human disorders by establishing the first explicit models of human neurodegenerative disease in C. elegans. In the last few years, our laboratory has primarily focused on delineating the cellular and molecular pathways that play critical roles in Amyotrophic Lateral sclerosis (ALS), Frontotemporal Dementia (FTD), and Huntington's Disease (HD).
Our laboratory undertakes behavioral, molecular, and genetic studies to understand the conserved mechanisms underlying behavior. Past work focused on how animals respond to changes in the environment. This resulted in the identification of a new family of conserved Notch co-ligands in C. elegans that play diverse roles regulating stress response. Current research examines the conserved molecular pathways that regulate sleep and fatigue.
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To understand why de novo mutations cause symptoms in patients with Alternating Hemiplegia of Childhood, we have developed C. elegans knock-in models for AHC by inserting patient missense mutations into the C. elegans eat-6 gene. C. elegans AHC model animals have dominant defects in synaptic function and we are focused on identifying cellular pathways that are responsible for these defects.