Thesis (Ph. D.)--University of Missouri--Columbia, 2001. / "December 2001." Typescript. Vita. Includes bibliographical references (leaves 228-272). Also available on the Internet.

Thesis (M.S.)--University of Tennessee Health Science Center, 2008. / Title from title page screen (viewed on July 31, 2008). Research advisor: Martha M Howe, Ph.D. Document formatted into pages (vii, 127 p. : ill.). Vita. Abstract. Includes bibliographical references (p. 103-116).

Thesis (Ph. D.)--University of Missouri--Columbia, 2000. / "December 2000." Typescript. Vita. Includes bibliographical references (leaves 133-147). Also available on the Internet.

Thesis (Ph. D.)--University of Missouri--Columbia, 2001. / Typescript. Vita. Includes bibliographical references (leaves 228-272). Also available on the Internet.

Dissertation (Ph.D.)--University of Toledo, 2007. / "In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Sciences." Title from title page of PDF document. Bibliography: p. 72-96.

Thesis (Ph.D.) -- University of Texas Southwestern Medical Center at Dallas, 2005. / Partial embargo. Vita. Bibliography: 154-191.

Thesis (Ph. D.)--University of Missouri--Columbia, 2000. / Typescript. Vita. Includes bibliographical references (leaves 133-147). Also available on the Internet.

Transcription by RNA polymerase II is a highly regulated process requiring a number of general and promoter specific transcription factors. Although many of the factors involved in the transcription reaction are known, exactly how they function to stimulate or repress transcription is not well understood. Central to understanding gene regulation is understanding the mechanism by which promoter specific transcription activators (activators) stimulate transcription. A group of factors called coactivators have been shown to be required for activator function in vitro. The best characterized coactivators to date are members of the TFIID complex. TFIID is a multisubunit complex composed of the TATA box binding protein (TBP) and 8-12 TBP associated factors (TAFIIs). Results from numerous in vitro experiments indicate that TAFIIs function by binding to activators and forming a bridge between the activator and the basal transcription machinery. In order to gain insight into the mechanism by which activators stimulate transcription, we chose to analyze the in vivo function of TAFIIs, their proposed targets. Results from the genetic disruption of a number of TAFIIs in the yeast Saccharomyces cerevisiae showed that most are encoded by essential genes. In order to study their function, temperature-sensitive and conditional alleles were constructed. Cells depleted of individual TAFIIs by either of these two methods displayed no defect in global transcription activation. Inactivation of yTAFII17, however, resulted in a promoter specific defect. In addition, inactivation of yTAFII145, yTAFII90, or TSM1, resulted in an inability of cells to progress through the cell-cycle. In an attempt to identify genes whose expression required yTAFII90, we performed subtractive hybridization on strains containing wild-type and temperature-sensitive alleles. Although this technique successfully identified genes differentially expressed in the two strains, it failed to identify genes whose expression required yTAFII90. These results indicate that TAFIIs are not the obligatory targets of activators, and that other factors must provide this role in vivo. Furthermore, that many of TAFIIs are required for cell-cycle progression.