Subcellular Localization of FAM171B in Mouse Neurons
Location
CSU Ballroom
Start Date
10-4-2018 10:00 AM
End Date
10-4-2018 11:30 AM
Student's Major
Biological Sciences
Student's College
Science, Engineering and Technology
Mentor's Name
Geoffrey Goellner
Mentor's Department
Biological Sciences
Mentor's College
Science, Engineering and Technology
Second Mentor's Name
Maddi Bauer
Second Mentor's Department
Biological Sciences
Second Mentor's College
Science, Engineering and Technology
Description
Huntington's disease (HD) is a severe neurodegenerative disorder for which there is no known cure. HD is one amongst a group of nine neurodegenerative diseases that all share a similar type of mutation. All of these diseases are defined by repeats of CAG (CAG codes for amino acid glutamine) within their DNA sequences, and in disease affected individuals these glutamine (Q) repeat tracts somehow expand beyond their normal range, resulting in cell death within specific subpopulations of neurons in each respective disease. The absence of expanded polyQ sequences in healthy populations has led to the inference that these mutated polyQ stretches are the primary cause of the pathological effects underlying HD and the other polyQ diseases. Numerous polyQ proteins have been identified, but have yet to be functionally characterized. One such novel polyQ protein that has yet to be extensively studied is FAM171B, and our lab has preliminary data showing its ubiquitous expression throughout mouse brain. In this study, we utilized immunofluorescence (IF) to reveal FAM171B's subcellular localization. IF was performed on neurons isolated from mouse brain tissue (BrainBits). Early microscopy data shows dense perinuclear localization of FAM171B as well as expression extending along neuronal processes. Experiments utilizing NeuN, a neuronal marker that will serve as a double label to ensure we are looking at neurons, are currently underway in our lab.
Subcellular Localization of FAM171B in Mouse Neurons
CSU Ballroom
Huntington's disease (HD) is a severe neurodegenerative disorder for which there is no known cure. HD is one amongst a group of nine neurodegenerative diseases that all share a similar type of mutation. All of these diseases are defined by repeats of CAG (CAG codes for amino acid glutamine) within their DNA sequences, and in disease affected individuals these glutamine (Q) repeat tracts somehow expand beyond their normal range, resulting in cell death within specific subpopulations of neurons in each respective disease. The absence of expanded polyQ sequences in healthy populations has led to the inference that these mutated polyQ stretches are the primary cause of the pathological effects underlying HD and the other polyQ diseases. Numerous polyQ proteins have been identified, but have yet to be functionally characterized. One such novel polyQ protein that has yet to be extensively studied is FAM171B, and our lab has preliminary data showing its ubiquitous expression throughout mouse brain. In this study, we utilized immunofluorescence (IF) to reveal FAM171B's subcellular localization. IF was performed on neurons isolated from mouse brain tissue (BrainBits). Early microscopy data shows dense perinuclear localization of FAM171B as well as expression extending along neuronal processes. Experiments utilizing NeuN, a neuronal marker that will serve as a double label to ensure we are looking at neurons, are currently underway in our lab.
Recommended Citation
Jones, Brooke. "Subcellular Localization of FAM171B in Mouse Neurons." Undergraduate Research Symposium, Mankato, MN, April 10, 2018.
https://cornerstone.lib.mnsu.edu/urs/2018/poster-session-A/8
