Thesis (Ph. D.)--University of Wisconsin--Madison, 1975. / Typescript. Vita. Description based on print version record. Includes bibliographical references (leaves 207-218).

No description available.

Thesis (Ph.D.)--University of Adelaide, Dept. of Molecular Biosciences, 2002? / Errata pasted onto back page. Bibliography: p. 133-149.

No description available.

Cytokinesis is the physical partition of one cell into two. In Chapter 1, I provide a brief introduction to cytokinesis and some of the proteins whose functions I parse out throughout my studies. In Chapter 2, I present work I’ve contributed to elucidate the role of polarity proteins in cytokinesis, as well as a look at the differential requirement for canonically essential cytokinetic proteins in the 4-cell embryo. In Chapter 3, I address a long-standing controversy in the field regarding the relationship between the Rac GAP protein Cyk-4 and the small GTPase Rac, and in particular the inhibitory role of Rac during cell division. My major body of work highlights the necessity not to close the books on the GAP activity of Cyk-4 and its inhibition of Rac. I show that Rac is unable to rescue cytokinesis failure in downstream Rho effectors whose loss weakens the contractile ring, suggesting it is not a promiscuous suppressor of cytokinesis. Additionally, I found that levels of non-muscle myosin-II and the actin binding domain of Utrophin were unchanged with loss of Cyk-4. From this, I infer that Cyk-4 is unlikely to be an activator of the RhoGEF Ect-2. These results emphasize the need to probe further into the cross-talk between these GTPases. In chapter 4, I show inconclusive data addressing the role of cell fate signaling in protection against cytokinesis failure. Overall, this thesis represents my contributions to the field, revealing the complexity involved in assuring successful completion of cytokinesis.

Thesis (M.S.)--University of Missouri--Rolla, 2007. / Vita. The entire thesis text is included in file. Title from title screen of thesis/dissertation PDF file (viewed December 7, 2007) Includes bibliographical references (p. 28-35).

No description available.

No description available.

Chlamydia trachomatis is the leading cause of bacterial sexually transmitted infections worldwide and it has been linked to increased risks of cervical cancer. Our study aims to understand the mechanisms by which chlamydia infection contributes to higher risks of tumorigenesis. We discovered in over 90% of infected human epithelial cells that chlamydia inclusions localized to the host cell centre during mitosis and prevented the completion of cleavage furrow ingression. Infected cells that failed to divide into two daughter cells re-entered interphase as tetraploid multinuclear cells, which are known initiators of tumorigenesis. In order to address whether chlamydia actively sought the host cell centre during mitosis, we created vacuoles using internalized latex beads and our findings indicated that chlamydia inclusions localized to the host cell centre much more frequently than similarly sized vacuoles. In addition, we demonstrated that metabolically inactive chlamydia inclusions localized to the cell centre less frequently than inclusions under normal conditions. Together, these results suggested that chlamydia actively localized to the host cell centre to efficiently block host cell mitosis. We took advantage of the microtubule-displacing capability of the C. trachomatis inclusions and demonstrated that astral microtubules could promote furrow initiation independent of the central spindle microtubules. Microdomains on chlamydia inclusions play important roles in inclusion localization and chlamydia replication. We discovered that these structures were surprisingly resistant to bacterial protein synthesis and host Src family kinase inhibitors. Finally, we demonstrated that multinuclear cells that resulted from unsuccessful mitosis contained significantly higher Golgi content, an important nutrient source for chlamydia. Our results indicated that C. trachomatis in multinuclear cells intercepted Golgi-derived lipids faster than in mononuclear cells. Together, my results reveal that C. trachomatis inclusions robustly localize to the cell centre to block host cell mitosis in order to acquire host Golgi nutrients more quickly in multinucleated cells.

Thesis (M.S.)--Missouri University of Science and Technology, 2008. / Vita. The entire thesis text is included in file. Title from title screen of thesis/dissertation PDF file (viewed January 22, 2009) Includes bibliographical references (p. 34-40).