Neurodegeneration is the progressive loss of neuron structures and functions, through which animals transmit information to and within the body. Today, about 5.4 million Americans are living with Alzheimer’s, the neurodegenerative disease, the sixth leading cause of death in the United States. The nematode, Caenorhabditis elegans, is an ideal model to study the genetic basis of neurodegenerative diseases because of its rapid life cycle and transparent body.
In C. elegans, the daf-19 gene encodes at least two functional proteins: DAF-19C and DAF-19A/B. DAF-19C, a smaller protein, is expressed in ciliated neurons and is a transcription factor vital for the development of sensory cilia. DAF-19A/B, a larger protein, is expressed in all non-ciliated neurons and plays a role in maintaining proper synaptic function. C.elegans lacking DAF-19A/B have behavioral and pharmacological abnormalities due to neurodegeneration as worms age. The goal of my research is to identify a portion of the cell machinery that maintains nerve cell function during aging, more specifically, to understand the role of the DAF- 19A/B in maintaining synaptic transmission.
Previous research identified 177 genes that may be dependent on the DAF-19 transcription factors; my research focuses on three of these genes, hex-1, tag-123, and F57B10.9. Using gene fusions with Green Fluorescent Protein (GFP), I tracked the location and amount of GFP produced when each gene is expressed to determine which cells (and which neurons) express each of the three genes. Using fluorescence microscopy, I found all three genes are expressed in neuronal tissues and are differently expressed in wild type vs. daf-19 mutant worms. These data suggest that DAF-19 controls expression of these genes, thus they maybe involved in synaptic maintenance.
Level of Honors
Elizabeth De Stasio
Korzynski, Jessica, "Investigating Neuronal Protein Regulation by daf-19: A Genetic Approach" (2012). Lawrence University Honors Projects. Paper 21.