Event Title
Effect of Normal Polyglutamine Polymorphism on Huntington Disease Protein Function.
Location
CSU Ballroom
Start Date
28-4-2009 10:00 AM
End Date
28-4-2009 12:00 PM
Student's Major
Biological Sciences
Student's College
Science, Engineering and Technology
Mentor's Name
Geoffrey M. Goellner
Mentor's Department
Biological Sciences
Mentor's College
Science, Engineering and Technology
Description
Huntington Disease (HD) is a progressive neurodegenerative disorder that causes deterioration of specific brain cells- leading to uncontrolled movement, emotional disturbance, and ultimately death. HD results from a mutation in the DNA encoding the protein huntingtin- a large protein of unknown fiinction ubiquitously expressed throughout all tissues of the human body. Interestingly, huntingtin contains a polyglutamine (polyQ) tract near its NH2-terminus that is normally polymorphic within the human population (Qe- Qss), but that increases in size well beyond its normal range to cause disease. It is unclear what consequence normal polyQ polymorphism has on huntingtin function within cells- thus we are deriving a series of HD constructs differing in polyQ tract length (to go along with the huntingtin constructs 23, 45, 55, and 86 glutamines currently in the lab). These new "normal range" constructs will ultimately be used to perform protein localization experiments within tissue culture cells to elucidate how normal polyQ tract length polymorphism affects huntingtin intracellular localization.
Effect of Normal Polyglutamine Polymorphism on Huntington Disease Protein Function.
CSU Ballroom
Huntington Disease (HD) is a progressive neurodegenerative disorder that causes deterioration of specific brain cells- leading to uncontrolled movement, emotional disturbance, and ultimately death. HD results from a mutation in the DNA encoding the protein huntingtin- a large protein of unknown fiinction ubiquitously expressed throughout all tissues of the human body. Interestingly, huntingtin contains a polyglutamine (polyQ) tract near its NH2-terminus that is normally polymorphic within the human population (Qe- Qss), but that increases in size well beyond its normal range to cause disease. It is unclear what consequence normal polyQ polymorphism has on huntingtin function within cells- thus we are deriving a series of HD constructs differing in polyQ tract length (to go along with the huntingtin constructs 23, 45, 55, and 86 glutamines currently in the lab). These new "normal range" constructs will ultimately be used to perform protein localization experiments within tissue culture cells to elucidate how normal polyQ tract length polymorphism affects huntingtin intracellular localization.
Recommended Citation
Thompson, Mark. "Effect of Normal Polyglutamine Polymorphism on Huntington Disease Protein Function.." Undergraduate Research Symposium, Mankato, MN, April 28, 2009.
https://cornerstone.lib.mnsu.edu/urs/2009/poster-session-C/4
