28th Annual Student Research Conference
Upregulation of the Minor Spliceosome in Mouse Retinae due to Zaprinast Exposure
Daniel R. Kick
Dr. Rahul Kanadia (University of Connecticut) and Dr. Elisabeth A. Hooper, Faculty Mentors
Eukaryotic genes require removal of non-coding stretches within coding regions to produce functional mRNAs. Splicing an intron is done by either the U2 or U12 spliceosome. This research focuses on the latter, which is of interest because it is highly conserved and because a mutation resulting in a nonfunctional U12 spliceosome is responsible for the developmental disease Microcephalic Osteodysplastic Primordial Dwarfism type 1. The specific roles of the U12 spliceosome are not well understood. To probe this system, we employed the retina as a model system, and used the snRNAs of the U12 spliceosome to measure up-regulation. Some genes known to impact cellular stress response have introns spliced by the U12 system. We administered a chemical agent, Zaprinast, to induce cellular stress in the retina. We found the snRNAs of the U12 spliceosome were found to be up-regulated in the experimental group suggesting a connection to regulating cellular stress response.
Keywords: U12 Spliceosome, Cellular stress response, Zaprinast
Topic(s):Biology
Presentation Type: Oral Paper
Session: 107-1
Location: MG 2001
Time: 8:00