Skip to Main Content
 

Global Search Box

 
 
 
 

Files

ETD Abstract Container

Abstract Header

Cytoskeletal Architecture and Cell Motility Remain Unperturbed in Mouse Embryonic Fibroblasts from Plk3 Knockout Mice.

Michel, Daniel R.

Abstract Details

2015, PhD, University of Cincinnati, Medicine: Molecular Genetics, Biochemistry, and Microbiology.
Polo-like kinase 3 (Plk3) is a member of a conserved family of serine/threonine kinases that primarily regulate cell cycle progression and mitotic events. In response to ionizing radiation, Plk3 facilitates the activation of G1/S checkpoint arrest. Further, published data from our lab suggested that Plk3 may be capable of activating G1/S checkpoint arrest independent of p53 signaling. The tumor suppressor protein p53 is the central hub of DNA damage response signaling and the most frequently deleted or mutated gene in cancers. A Plk3-dependent, p53-independent mechanism for G1/S checkpoint arrest could partially compensate for the loss of p53 function. Therefore, in our first project, we investigated the hypothesis that the combined loss of p53 and Plk3 would be synthetic lethal with cell death resulting from the abolishment of the G1/S checkpoint and the accumulation of unrepaired DNA damage. However, our experimental results did not support our hypothesis and we decided to shift to a new project. The Plk literature also suggests that Plk3 may have additional roles associated with normal cell function. Here, mouse embryonic fibroblasts generated from Plk3 knockout or wildtype mice were compared, to identify alternative functions for Plk3 in addition to its canonical role. Specifically, Plk3 has been reported to associate with key proteins involved in cytoskeletal organization; co-localizing with f-actin and directly phosphorylating ß-tubulin. These and other data suggested a role for Plk3 in regulation of the cytoskeleton and cell morphology. To this end, given the importance of dynamic cytoskeletal rearrangement to cell motility, we analyzed whether Plk3 is involved in cell migration, attachment and/or invasion using Plk3 knockout mouse embryonic fibroblasts.
Peter Stambrook, Ph.D. (Committee Chair)
El Mustapha Bahassi, Ph.D. (Committee Member)
Rhett Kovall, Ph.D. (Committee Member)
Anil Menon, Ph.D. (Committee Member)
William Miller, Ph.D. (Committee Member)
78 p.

Recommended Citations

Citations

  • Michel, D. R. (2015). Cytoskeletal Architecture and Cell Motility Remain Unperturbed in Mouse Embryonic Fibroblasts from Plk3 Knockout Mice. [Doctoral dissertation, University of Cincinnati]. OhioLINK Electronic Theses and Dissertations Center. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1446546516

    APA Style (7th edition)

  • Michel, Daniel. Cytoskeletal Architecture and Cell Motility Remain Unperturbed in Mouse Embryonic Fibroblasts from Plk3 Knockout Mice. 2015. University of Cincinnati, Doctoral dissertation. OhioLINK Electronic Theses and Dissertations Center, http://rave.ohiolink.edu/etdc/view?acc_num=ucin1446546516.

    MLA Style (8th edition)

  • Michel, Daniel. "Cytoskeletal Architecture and Cell Motility Remain Unperturbed in Mouse Embryonic Fibroblasts from Plk3 Knockout Mice." Doctoral dissertation, University of Cincinnati, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1446546516

    Chicago Manual of Style (17th edition)