Function of UCHL1 Gene in Neurons using TALEN-mediated Mutagenesis

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Horton, Mary
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Symposium on Undergraduate Research and Creative Expression
Iowa State University Conferences and Symposia

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.

Genetics, Development and Cell Biology

Amyotrophic lateral sclerosis (or Lou Gehrig's disease) is a neurodegenerative disease caused by the death of motor neurons in the spinal cord and the brain. Once these nerve cells die, the patient's muscle cells degenerate, resulting in paralysis and eventually death. Most cases of ALS are sporadic, meaning that a clear molecular and genetic understanding of the mechanisms by which the motor neurons die is lacking. Ubiquitin C-terminal hydrolase-L1 (UCHL1) is one gene that has been implicated in ALS, as well as several other neurodegenerative diseases. To gain a better understanding into the function of UCHL1 in non-diseased neurons, we are using TAL-effector nucleases (TALEN) to create UCHL1 mutant zebrafish. Specifically, I have generated these TALENs and begun to inject them to generate the mutant fish. Once created, these fish will provide insights into the normal function of UCHL1 and, hopefully, allow us to create a new zebrafish model of nerve cell degeneration.

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