My name is Helen Heo, and I am an undergraduate at the University of Wisconsin-Madison majoring in Molecular Biology and Neurobiology. At UW-Madison, I work in the lab of Dr. Darcie Moore, studying asymmetric segregation in mitotic neural stem cells. The Moore Lab is broadly interested in stem cell aging and how stem cells may maintain “youthfulness.” Last summer, I also worked in the lab of Dr. Chun-Li Zhang at the University of Texas Southwestern, examining the role of Nrf2 and p62 in induced motor neurons from human ALS patients.
Through the SENS Research Foundation Summer Scholars Program, I worked in Dr. Jennifer Garrison’s lab at the Buck Institute for Research on Aging. The Garrison Lab uses the nematode worm C. elegans and mouse models to investigate cellular and circuit mechanisms of neuropeptide signaling and how they may change with age. Neuropeptides are secreted molecules that facilitate long-distance communication between neurons and between the brain and periphery, acting like the brain’s wifi.
Intermediate filaments (IFs) are one of the three cytoskeletal systems. They are found and play important roles in nearly all cells in vertebrates and have been implicated in disease and aging. Several diseases are associated with mutations in IF proteins, including Parkinson’s disease, amyotrophic lateral sclerosis (ALS), Hutchinson-Gilford progeria syndrome, and dominant cataracts. We are particularly interested in the intermediate filament vimentin. Previous studies in in vitro and in vivo mouse models suggest that vimentin is involved in proteostasis (protein regulation), stress response, and aging, and that loss of vimentin may confer negative consequences in situations of stress and possibly aging.
Accordingly, I will use C. elegans to investigate the role of vimentin in stress and aging in vivo. C. elegans provide an ideal system to do so with a short lifespan, ease of genetic manipulation, and several stress-inducing paradigms. C. elegans have 11 intermediate filament genes, and very little is known about the role of intermediate filaments in C. elegans. We have obtained mutant C. elegans strains for each of five vimentin candidate intermediate filament genes. Using these strains, I plan to: (1) investigate the role intermediate filaments play in stress; (2) examine how intermediate filaments are involved in aging; and (3) identify a vimentin homolog in C. elegans for future studies. Future studies of a vimentin homolog in C. elegans may elucidate the role of intermediate filaments in age-related diseases involving protein aggregation, such as Parkinson’s Disease, Alzheimer’s Disease, and Huntington’s Disease.