Gail Johnson, PhD
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Affiliation(s):
University of Rochester Medical Center
ORCID URL:
Areas of Interest:
tau, endolysosome pathway, autophagy, effects of pathological tau on mitochondrial biology.
Biography & Research:
I have had a longstanding interest in tau biology. When I was a postdoctoral fellow at the University of Alabama at Birmingham (UAB) in the late 80’s I developed an interest in protein phosphorylation and how it regulates the function of cytoskeletal proteins. Serendipitously, Dr. Lester (Skip) Binder was faculty at UAB and had recently published a paper on the abnormal tau phosphorylation in Alzheimer’s disease brain, so I went to meet with him. His passion for tau was contagious and I was hooked, over the next year I basically camped out in his lab and learned all I could about tau and tau phosphorylation. We published a paper together (1989), my first paper on tau. We remained in close contact and interacted regularly in the years that followed, even after he left UAB. He was my “go to” person when I had questions about tau until the sad day in 2013 when he passed away unexpectedly. I still miss him. Nonetheless, I have stayed focused on tau and have been very productive. My studies have been supported by the NIH for almost 30 years and I have published more than 100 papers on tau, and continue to be committed to understanding tau biology. I have given many talks both nationally and internationally on tau, and organized symposia on tau. We have supplied many labs with our numerous tau constructs, and are fully committed to sharing our resources. Over the past 10 years my research has been focused on defining the processes that regulate tau clearance, and recently with an increased emphasis on understanding the molecular mechanisms that regulate vacuolar dependent degradation systems and the role they play in maintaining neuronal proteostasis.
In addition, we also have developed an interest in understanding how specific pathological forms of tau cause toxicity. For these studies we have begun to use C. elegans as our model system to express single copies of specific tau mutants to understand the impact on neuronal health in general and mitochondrial biology more specifically. Overall, the long range goals of our studies are to understand the molecular processes that regulate neuronal, vacuolar-dependent degradative systems, and how dysregulation of these processes contribute to the initiation and progression of tauopathies. Further, we are focused on delineating the mechanisms by which pathological tau species exert their toxicity with a focus on mitochondrial dynamics and function.
