Publication No. _______

Dedication This is dedicated to my fiancé, Paul, and my loving family for their endless support and encouragement. v Acknowledgements I would like to thank my fiancé, my family, and my friends who all supported me during my years of studies. I would like to thank all the members of the Tucker lab who helped me become the scientist I am today. I would especially like to thank Loren Probst and Chhaya Das who have provided me with invaluable information throughout the years. Without their help this project would not be where it is today. I would like to that Grace Kubin who welcomed me into the lab and mentored me through my rotation project. I would especially like to thank my mentor, Dr. Phil Tucker, for all his help and patience. Lastly, I would like to thank the University of Texas for the resources I needed to complete my project. ARID proteins are highly conserved among eukaryotes and are involved in chromatin remodeling, differentiation and development. The founding member of the ARID3 subfamily, Bright/ARID3A, is an activator of the immunoglobulin heavy chain locus. Bright has been shown to immortalize mouse embryonic fibroblasts and induce malignant transformation when co-expressed with oncogenic Ras. A genomic locus that encodes a gene paralogous to Bright has been identified as Brightlike/ARID3C. In addition to the highly conserved ARID and REKLES domains, Brightlike contains a conserved sumoylation motif. Brightlike orthologous genes have been identified in all vertebrate genomes examined. Its absence from EST databases suggested that it is a rare transcript, and accordingly, its expression in adult mice appears to be restricted to spleen, testes and thymus. Brightlike is also regulated by alternative pre-mRNA splicing, differential subcellular distribution, and post-translational modification by SUMO. The two isoforms of Brightlike appear to have differential expression in lymphocyte populations. Brightlike and Bright bind to the same DNA motif. Unexpectedly, Bright vii and Brightlike do not form heterocomplexes on DNA nor compete for binding, suggesting they have independent functions in vivo. Brightlike increases the proliferation potential of mouse embryonic fibroblasts and rescues cells from premature senescence, suggestive of a proto-oncogene.

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