Non-Coding RNA in Muscular Dystrophy
School Name
South Carolina Governor's School for Science and Mathematics
Grade Level
12th Grade
Presentation Topic
Cell and Molecular Biology
Presentation Type
Mentored
Abstract
Duchenne Muscular Dystrophy (DMD) is caused by the lack of dystrophin protein, which protects muscle cells from shock and damage. One of the most common dystrophy disorders, DMD currently has no cure and has a life expectancy around 28. Previous research has shown that Utrophin, a protein with a near identical structure and function, is capable of replacing dystrophin and sparing muscles from DMD. Mice who had both their gene for Utrophin and Dystrophin silenced were expected to show complete symptoms for the disorder. Instead, some mice showed immunity to DMD in specific parts of their body. It is believed that the damaged exons of the Utrophin gene were related to the production of the protein. We found that exon 7 in the utrophin gene was still intact in mice with immunity to the disorder and that the exon was transforming into the circular RNA. Our research dealt with these exons by investigating what kind of mechanism could have created the protein, and how it was possible for the circ-RNA toinfluence the expression of the disorder. This Circ-RNA is believed to be the deciding factor in whether patients lacking dystrophin are affected by DMD or not. Our research specifically dealt with the transfection of plasmids into cells, RNA purification, and Western blots in order to understand how the circ-RNA containing exon 7 is stabilized within cells. By understanding how the RNA is stabilized, we can begin to learn how it behaves within cells.
Recommended Citation
Palmera, Juliana, "Non-Coding RNA in Muscular Dystrophy" (2023). South Carolina Junior Academy of Science. 15.
https://scholarexchange.furman.edu/scjas/2023/all/15
Location
ECL 104
Start Date
3-25-2023 9:45 AM
Presentation Format
Oral Only
Group Project
No
Non-Coding RNA in Muscular Dystrophy
ECL 104
Duchenne Muscular Dystrophy (DMD) is caused by the lack of dystrophin protein, which protects muscle cells from shock and damage. One of the most common dystrophy disorders, DMD currently has no cure and has a life expectancy around 28. Previous research has shown that Utrophin, a protein with a near identical structure and function, is capable of replacing dystrophin and sparing muscles from DMD. Mice who had both their gene for Utrophin and Dystrophin silenced were expected to show complete symptoms for the disorder. Instead, some mice showed immunity to DMD in specific parts of their body. It is believed that the damaged exons of the Utrophin gene were related to the production of the protein. We found that exon 7 in the utrophin gene was still intact in mice with immunity to the disorder and that the exon was transforming into the circular RNA. Our research dealt with these exons by investigating what kind of mechanism could have created the protein, and how it was possible for the circ-RNA toinfluence the expression of the disorder. This Circ-RNA is believed to be the deciding factor in whether patients lacking dystrophin are affected by DMD or not. Our research specifically dealt with the transfection of plasmids into cells, RNA purification, and Western blots in order to understand how the circ-RNA containing exon 7 is stabilized within cells. By understanding how the RNA is stabilized, we can begin to learn how it behaves within cells.
