On a fateful afternoon at the beginning of my sophomore year, I had no idea that walking into Dr. Johnson’s office with what I thought was a simple question about sleep would lead to a multi-year endeavor to answer. Over the course of this project, I’ve learned that science and scientific discovery is not as straight forward as my schooling has lead me to believe. Science is a dough that you must knead over and over again and when you fail, you must try another strategy. I had to get back up on several occasions which put my problem solving and patience to the test. With the rise of covid-19 at my university, LSU students had been told to leave campus and research activity was halted. From this, I ultimately ended up losing my sleep deprivation model because my research requires constant maintaining due to the nature of fly genetics. I have a substantial amount of data on my sleep deprivation model and am now looking to use my characterization of my model as my Honors Thesis.

My model uses and optogentic caspase strategy to target and destroy fly sleep neurons with a binary expression system via natural apoptosis. My mentor and I examined other approaches such as mechanical rotation that ultimately were ineffective for our needs. Due to Covid-19, my Honors Thesis has since shifted in an unpredictable manner, but I still retain hope in continuing my research where I left off at a later date. From this experience, I have learned how research and data analysis is conducted, how to communicate and demonstrate my science to a variety of audiences of varying aptitudes, and found a deep appreciation for the scientific work that those before me have accomplished.

Below is my virtual presentation and abstract at LSU Discover Day 2020 along with my presentation at the LSU College of Science 2019 Science & Spirits Alumni event

Using a Drosophila optogenetic model to identify factors that suppress negative effects of sleep deprivation

The conservation of sleep suggests it maintains vital functions for survival; however, many segments of adult populations, such as night-shift workers and college students, suffer from cumulative partial sleep deprivation while roughly one-third of the adult population experiences significant sleep loss. Loss of sleep has shown to cause various consequences, such as impairments in cognitive, motor, metabolic, hormonal, immunological, and behavioral performances. Recently, we found that the sleep driver GR23E10 – Gal4 in conjunction with a gene that initiates natural cellular apoptosis is effective in reducing the overall sleep of the organism. Using the model organism Drosophila melanogaster, we found that a 10 – 20% reduction in total acquired sleep causes a significant decrease in organismal longevity. The restorative function of sleep is thought to be a consequence of enhanced removal of neurotoxic waste products accumulated during the awake state nervous system via increased autophagy activity by intracellular lysosomes (Ellenbogen, 2005; Hara et al., 2006; Xle et al., 2013). Valosin-containing protein (VCP) is known to participate in organelle formation, such as lysosomes in muscles, Golgi Apparatus, Endoplasmic Reticulum, and the nuclear envelope (Zhang et al., 1994; Latterich et al., 1995; Rabouille et al., 1995; Lavoie et al., 2000; Roy et al., 2000; Hetzer et al., 2001). The small p97/VCP-interacting protein (SVIP) both inhibits the endoplasmic reticulum associated degradation pathway and leads to the localization of VCP at various locations within the cell when overexpressed (Nagahama et al., 2003; Wang et al., 2011). Collectively, these findings indicate that overexpression of SVIP will consequentially enhance VCP activity and improve lysosomal maintenance which could induce improved health benefits. Further analysis of this overexpression of SVIP within sleep deprived fruit flies will likely shed light on the role of lysosomal activity within sleep’s restorative functions while providing relevant information on the consequences of VCP and SVIP on lysosome regulation and activity.

The Johnson Lab

The Johnson lab uses invertebrate model organisms (fruit flies and worms) to explore the genetic and molecular causes of age-related degenerative diseases, such as ALS, Alzheimer’s and Parkinson’s disease. A common feature of many degenerative diseases is the progressive accumulation of protein aggregates. Autophagy-lysosome mediated degradation is the major pathway that clears aggregates from the cytoplasm and autophagy defects are associated with many degenerative diseases. We use a combination of genetic, biochemical and microscopy methods to study the autophagy-lysosome system in both healthy and disease contexts. Additionally, we are exploring natural mechanisms that enhance proteostasis as a potential therapeutic approach to combat neurodegenerative diseases.