Title

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.

Location

ECL 104

Start Date

3-25-2023 9:45 AM

Presentation Format

Oral Only

Group Project

No

COinS
 
Mar 25th, 9:45 AM

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.