Title

The Role of the Skp2-CyclinA Interaction in Drosophila Cell Cycle Regulation

Submitter and Co-author information

Kawmadi Abeytunge, University of WindsorFollow

Type of Proposal

Oral presentation

Streaming Media

Faculty

Faculty of Science

Faculty Sponsor

Andrew Swan

Abstract/Description of Original Work

The cell cycle is a highly controlled process, requiring the role of several regulatory proteins to ensure proper cell division. One of these proteins is Skp2, a substrate recognition subunit of the SCF complex - a protein conglomerate required for the destruction of the tumour suppressor, p27/Dap. This role has long characterized Skp2 as a proto-oncogene, with the potential to interfere with normal cell regulation if overexpressed; however, Skp2 is also necessary for proper cell division, as the loss of Skp2 results in polyploidy of mitotically dividing cells. While most research on Skp2 has emphasized its role down-regulating p27, one study indicates that the knockdown of Skp2 might have an effect on other cell cycle regulators in a pathway independent of p27, causing polyploidy. However, these regulators that Skp2 affects, have not yet been fully clarified. Among important cell cycle regulators Skp2 interacts with is Cyclin A, a key protein in G2 regulation and mitotic entry in Drosophila. Like Skp2, Cyclin A is required for preventing polyploidy, indicating that Cyclin A is a point of interest in our study of Skp2. Moreover, previous studies show that the N-terminus of Skp2 interacts directly with Cyclin A in both Drosophila and mammals via a domain independent of SCF interaction; the N-terminus also happens to be required for rescuing polyploidy in Skp2 null mitotic cells. Thus, we predict that it is the Skp2-CycA interaction that is necessary for preventing polyploidy. To test this prediction, this project will aim to characterize the Skp2-CycA interaction in a Drosophila model through various immunochemistry techniques. Understanding this interaction in greater detail will enhance our knowledge of the cellular processes that are crucial for cell cycle regulation.

Start Date

31-3-2017 3:30 PM

End Date

31-3-2017 4:50 PM

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Mar 31st, 3:30 PM Mar 31st, 4:50 PM

The Role of the Skp2-CyclinA Interaction in Drosophila Cell Cycle Regulation

The cell cycle is a highly controlled process, requiring the role of several regulatory proteins to ensure proper cell division. One of these proteins is Skp2, a substrate recognition subunit of the SCF complex - a protein conglomerate required for the destruction of the tumour suppressor, p27/Dap. This role has long characterized Skp2 as a proto-oncogene, with the potential to interfere with normal cell regulation if overexpressed; however, Skp2 is also necessary for proper cell division, as the loss of Skp2 results in polyploidy of mitotically dividing cells. While most research on Skp2 has emphasized its role down-regulating p27, one study indicates that the knockdown of Skp2 might have an effect on other cell cycle regulators in a pathway independent of p27, causing polyploidy. However, these regulators that Skp2 affects, have not yet been fully clarified. Among important cell cycle regulators Skp2 interacts with is Cyclin A, a key protein in G2 regulation and mitotic entry in Drosophila. Like Skp2, Cyclin A is required for preventing polyploidy, indicating that Cyclin A is a point of interest in our study of Skp2. Moreover, previous studies show that the N-terminus of Skp2 interacts directly with Cyclin A in both Drosophila and mammals via a domain independent of SCF interaction; the N-terminus also happens to be required for rescuing polyploidy in Skp2 null mitotic cells. Thus, we predict that it is the Skp2-CycA interaction that is necessary for preventing polyploidy. To test this prediction, this project will aim to characterize the Skp2-CycA interaction in a Drosophila model through various immunochemistry techniques. Understanding this interaction in greater detail will enhance our knowledge of the cellular processes that are crucial for cell cycle regulation.