Event Title
Expression of a Mutant Form of a Human Dementia-Related Gene in the Drosophila Brain is Capable of Disrupting Circadian Rhythms
Location
Parker-Reed, SSWAC
Start Date
30-4-2015 9:00 AM
End Date
30-4-2015 10:55 AM
Project Type
Poster
Description
Frontotemporal dementia (FTD) is the second most common age correlated dementia. One protein implicated in FTD is CHMP2B, which when mutated can cause disruptions in the functioning of an ESCRT-III component. ESCRT proteins are required for the forming of multivesicular bodies, an important component of the endosomal-lysosomal pathway. Disruptions in this pathway are linked to numerous diseases including Huntingtons disease, amyotropic lateral sclerosis, and FTD. FTD, as well as many other neurodegenerative diseases, has been shown to disrupt the sleep-wake cycles of patients dictated by circadian rhythms. Here we show that misexpression of a mutant form of CHMP2B in the Drosophila nervous system using the GAL4-UAS system leads to disruption of circadian rhythms. We have also attempted to characterize the expression patterns of several circadian-rhythm driver lines so that in the future we may determine if the disruption is due to expression of CHMP2B in pacemaker cells. Specific results will be further discussed.
Sponsoring Department
Colby College. Biology Dept.
CLAS Field of Study
Natural Sciences
Event Website
http://www.colby.edu/clas
ID
1075
Expression of a Mutant Form of a Human Dementia-Related Gene in the Drosophila Brain is Capable of Disrupting Circadian Rhythms
Parker-Reed, SSWAC
Frontotemporal dementia (FTD) is the second most common age correlated dementia. One protein implicated in FTD is CHMP2B, which when mutated can cause disruptions in the functioning of an ESCRT-III component. ESCRT proteins are required for the forming of multivesicular bodies, an important component of the endosomal-lysosomal pathway. Disruptions in this pathway are linked to numerous diseases including Huntingtons disease, amyotropic lateral sclerosis, and FTD. FTD, as well as many other neurodegenerative diseases, has been shown to disrupt the sleep-wake cycles of patients dictated by circadian rhythms. Here we show that misexpression of a mutant form of CHMP2B in the Drosophila nervous system using the GAL4-UAS system leads to disruption of circadian rhythms. We have also attempted to characterize the expression patterns of several circadian-rhythm driver lines so that in the future we may determine if the disruption is due to expression of CHMP2B in pacemaker cells. Specific results will be further discussed.
https://digitalcommons.colby.edu/clas/2015/program/99