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Presentation Title

Evaluation Of Familial Mutants Of Parkinson's Protein Alpha-Synuclein: Unexpected A30P dominance in combination mutants

Student Presenter(s) and Advisor

Natalie Kukulka '13Follow

Location

Meyer Auditorium

Abstract

Genetic mutations account for 10% of familial Parkinson’s disease (PD). The best-studied gene is α-synuclein and its PD mutations change three amino acids (A53T, A30P and E46K). Each amino acid mutant affects α-synuclein’s properties in a distinct way. Yet, how they affect the other in governing α-synuclein's PD-related properties is unknown. In my senior thesis, I tested the hypothesis that each mutant contributes equally in exerting such influence. Specifically, I compared double and triple combination mutants with single mutants for localization, accumulation and toxicity in two yeast models. I discovered an unexpected dominance of A30P in both yeasts.

Presentation Type

Individual Presentation

Start Date

4-9-2013 10:20 AM

End Date

4-9-2013 10:40 AM

Panel

Panel: Frontiers of the Human Body

Panel Moderator

Jennifer Jeziorski

Field of Study for Presentation

Neuroscience

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Apr 9th, 10:20 AM Apr 9th, 10:40 AM

Evaluation Of Familial Mutants Of Parkinson's Protein Alpha-Synuclein: Unexpected A30P dominance in combination mutants

Meyer Auditorium

Genetic mutations account for 10% of familial Parkinson’s disease (PD). The best-studied gene is α-synuclein and its PD mutations change three amino acids (A53T, A30P and E46K). Each amino acid mutant affects α-synuclein’s properties in a distinct way. Yet, how they affect the other in governing α-synuclein's PD-related properties is unknown. In my senior thesis, I tested the hypothesis that each mutant contributes equally in exerting such influence. Specifically, I compared double and triple combination mutants with single mutants for localization, accumulation and toxicity in two yeast models. I discovered an unexpected dominance of A30P in both yeasts.