Publication Date
2016
Document Type
Thesis
Committee Members
Paula Bubulya (Advisor), Katherine Excoffon (Committee Member), Labib Rouhana (Committee Member)
Degree Name
Master of Science (MS)
Abstract
Serine-arginine-rich (SR) or SR-like splicing factors interact with exon junction complex proteins during pre-mRNA processing to promote mRNA packaging into mature messenger ribonucleoproteins (mRNPs) and to dictate mRNA stability, nuclear export, and translation. In this thesis, I examined if depletion of two homologous non-classical serine-arginine-rich (SR) splicing factors, Btf (BCLAF1) and TRAP150, impacts regulation of cell cycle regulator transcripts and mitosis. Previous work showed that depletion of these proteins by RNAi causes mitotic defects including chromosome misalignment in metaphase. However, since Btf and/or TRAP150 did not co-localize with mitotic structures during mitosis, I hypothesized that Btf and/or TRAP150 depletion affect mitosis indirectly through altered expression of mitotic regulator transcripts. My results indicated that Btf and TRAP150 are important for controlling the abundance of transcripts that encode mitotic regulators. My results also suggest that Btf and TRAP150 have increased effects in maintaining the alignment of chromosomes at metaphase, as co-depletion of Btf and TRAP150 showed increased effects on the misalignment of chromosomes, thus demonstrating an important role in mitotic progression. Future studies will determine if altered expression or processing of endogenous cell cycle regulator protein transcripts is a result of changes in transcript distribution, and they will tease apart the molecular mechanisms underlying defective mitotic chromosome alignment/segregation in absence of Btf and TRAP150.
Page Count
96
Department or Program
Department of Biological Sciences
Year Degree Awarded
2016
Copyright
Copyrigh 2016t, some rights reserved. My ETD may be copied and distributed only for non-commercial purposes and may not be modified. All use must give me credit as the original author.
Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 License.
