Parkinson’s Disease is a common neurodegenerative disease characterized by the death of dopaminergic neurons, which can be caused by oxidative stress in the mitochondria and subsequent DNA damage. It is known that the mutated variant of the LRRK2 gene causes Parkinson’s Disease; however, the role of the unmutated gene, outside of its kinase activity, is relatively unknown. We seek to determine the role of the unmutated LRRK2 gene under oxidative stress and DNA damage by simulating these conditions with toxins in both wild type and CRISPR edited LRRK2-KO cell lines. We will be using western blots to measure the differences in phosphorylated proteins known to respond to DNA damage and different levels of cyclins and related proteins that may contribute to the cessation of the cell cycle. We expect to find that the resistance to DNA damage and the percent of cell death is different in the two cell lines. We also expect to find that the LRRK2-KO cell line, under stressful conditions, creates a checkpoint in the cell cycle that stops growth and division. Understanding LRRK2’s role and its pathways can help us better understand how the increased kinase activity of the mutated gene causes Parkinson’s Disease.

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