Submission Date

7-24-2015

Document Type

Paper- Restricted to Campus Access

Department

Biology

Faculty Mentor

Rebecca Kohn

Comments

Presented during the 17th Annual Summer Fellows Symposium, July 24, 2015 at Ursinus College.

Supported by a Howard Hughes Medical Institute (HHMI) grant through the FUTURE Program.

Project Description

Oxidative stress in cells is caused by reactive oxygen species (ROS) if there is a deficiency of necessary antioxidants to neutralize them. ROS, that work through free radicals, oxidize sites on endogenous neurotransmitters and other important cellular components that allow cells to function properly. When cellular components are oxidized, they are unable to continue normal functioning and will eventually die through apoptosis. This cell death can contribute to the neurodegeneration seen in Parkinson’s disease. Increased intracellular dopamine allows more oxidation sites for ROS within the cell contributing to further neurodegeneration. It is believed that lower levels of dopamine within the cell can lead to a prolonged or inhibition of neurodegeneration which can be simulated using a mutation in the dopamine reuptake transporter. Within the model organism Caenorhabditis elegans crossed with GFP, one can visually determine the effects of low intracellular dopamine on neurodegeneration using a mutation in the dopamine transporter, dat-1. Attempts of the forward and reverse primer combination were unsuccessful; which led to the failure of the genetic cross of GFP and the dat-1 mutation. Future research will continue the cross using an internal primer to amplify DNA within the sequence deletion. Subsequently, gel electrophoresis allows visualization of the zygosity of the mutation. The dat-1 mutation with the GFP tag has not been finished at this time.

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