Assessing the role of the ALS-associated gene NEK1 in zebrafish motor neuron development
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The Symposium provides undergraduates from all academic disciplines with an opportunity to share their research with the university community and other guests through conference-style oral presentations. The Symposium represents part of a larger effort of Iowa State University to enhance, support, and celebrate undergraduate research activity.
Though coordinated by the University Honors Program, all undergraduate students are eligible and encouraged to participate in the Symposium. Undergraduates conducting research but not yet ready to present their work are encouraged to attend the Symposium to learn about the presentation process and students not currently involved in research are encouraged to attend the Symposium to learn about the broad range of undergraduate research activities that are taking place at ISU.
The first Symposium was held in April 2007. The 39 students who presented research and their mentors collectively represented all of ISU's Colleges: Agriculture and Life Sciences, Business, Design, Engineering, Human Sciences, Liberal Arts and Sciences, Veterinary Medicine, and the Graduate College. The event has grown to regularly include more than 100 students presenting on topics that span the broad range of disciplines studied at ISU.
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Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease associated with the loss of motor neurons, ultimately leading to death of the patient. In recent years, a significant number of genes associated with the disease have been discovered, but it is still unknown how mutations in these genes can cause ALS. My project works with genome editing technology in the zebrafish, Danio rerio, to study the effect on motor neuron development and degeneration by producing knock-out and knock-in mutations in the fish. In particular, I am focusing my work on the NEK1 gene, a recently-discovered gene that could be linked to a significant number of ALS cases. I am using the CRISPR/Cas9 system to generate a loss-of-function allele for NEK1, which can induce a mutation to make a nonfunctional protein. Then, I can use this mutation in the zebrafish to analyze the role that the NEK1 gene plays in motor neuron development and degeneration, specifically related to ALS symptoms. Furthermore, in the future, I will test the isolated effect of the p.Arg261His amino acid substitution to understand its specific role in ALS cases, particularly whether this gene contributes in a dominant or recessive manner to causing the disease.