Modified PNA Oligomers as a Method for Recognition of Mutant Non-Coding RNA
Location
Atrium
Session Format
Poster Presentation
Research Area Topic:
Natural & Physical Sciences - Chemistry
Co-Presenters and Faculty Mentors or Advisors
Dr. Arambula
faculty advisor
Abstract
Trinucleotide Repeat Expansion Disorders (TREDS) are ascribed to generational expansion of genomic repeats. In many cases, these genomic repeats are transcribed to non-coding regions at the RNA level resulting in novel loss of function mechanisms. In this presentation, we propose and present preliminary work on the ability of modified PNA oligomers as a means of RNA and DNA repeat recognition using CUG/CTG repeats (Myotonic Dystrophy type 1) as a model. We propose that by binding to the mutant RNA, the PNA would inhibit non-natural RNA-protein binding events at specific trinucleotide repeats which is considered to be the direct cause of myotonic dystrophy type 1. If efficient, the findings of this research may lead to a new class of compounds that will provide treatment for genetic diseases that are caused by mutant RNA.
Keywords
Myotonic dystrophy, Acridine, Peptide nucleic acid, Trinucleotide repeat expansion disorders
Presentation Type and Release Option
Presentation (Open Access)
Start Date
4-24-2015 2:45 PM
End Date
4-24-2015 4:00 PM
Recommended Citation
Ramirez, Alexandro, "Modified PNA Oligomers as a Method for Recognition of Mutant Non-Coding RNA" (2015). GS4 Georgia Southern Student Scholars Symposium. 97.
https://digitalcommons.georgiasouthern.edu/research_symposium/2015/2015/97
Modified PNA Oligomers as a Method for Recognition of Mutant Non-Coding RNA
Atrium
Trinucleotide Repeat Expansion Disorders (TREDS) are ascribed to generational expansion of genomic repeats. In many cases, these genomic repeats are transcribed to non-coding regions at the RNA level resulting in novel loss of function mechanisms. In this presentation, we propose and present preliminary work on the ability of modified PNA oligomers as a means of RNA and DNA repeat recognition using CUG/CTG repeats (Myotonic Dystrophy type 1) as a model. We propose that by binding to the mutant RNA, the PNA would inhibit non-natural RNA-protein binding events at specific trinucleotide repeats which is considered to be the direct cause of myotonic dystrophy type 1. If efficient, the findings of this research may lead to a new class of compounds that will provide treatment for genetic diseases that are caused by mutant RNA.
