Validating Drosophila melanogaster as a tool to investigate the Tuberin-Cyclin B1 interaction
Standing
Undergraduate
Type of Proposal
Oral Presentation
Faculty
Faculty of Science
Faculty Sponsor
Lisa Porter
Proposal
Cancer is a disease that can arise from uncontrolled division of cells when the cell cycle is not properly regulated. The cell cycle is composed of four distinct phases: G1, S, G2 and M. To preserve cellular integrity, the cell has checkpoints which must be fulfilled in order to pass through each of the phase. Each of these checkpoints is regulated by a cyclin-CDK complex. The G2/M checkpoint is regulated by a Cyclin B1-CDK1 complex in the nucleus. In late G2 phase, Cyclin B1 (CycB1) accumulates in the nucleus from the cytoplasm. The overexpression of CycB1 has been associated with tumor aggressiveness and, therefore, CycB1 may have the potential to be a new therapeutic target in many aggressive cancers. Tuberin is a tumor suppressor protein that can bind CycB1 in the cytoplasm to regulate entry of CycB1 into the nucleus during the G2/M transition. Research into the Tuberin and CycB1 interaction may be promising for the field of cancer research. The Porter lab has studied the Tuberin-CycB1 interaction in vitro using established cell lines, but no one to date has studied this using an in vivo model which would provide us with more in-depth information about disease models. This project focuses on validating the Drosophila melanogaster as a model to study the Tuberin-CycB1 interaction. Drosophila melanogaster offers the unique advantage of having short generation times to permit high-throughput data to be collected. Moreover, the imaginal discs in the eye and wing of Drosophila contain regions of cells that are synchronized in the various phases of the cell cycle, providing the advantage that results can be seen at every phase of the cell cycle using this system. Our goal for this project is to first develop and validate a Drosophila disease model for Tuberin-CycB1 interactions and use it to gain more insight on possible targeted treatments for cancer using CyclinB1.
Grand Challenges
Viable, Healthy and Safe Communities
Validating Drosophila melanogaster as a tool to investigate the Tuberin-Cyclin B1 interaction
Cancer is a disease that can arise from uncontrolled division of cells when the cell cycle is not properly regulated. The cell cycle is composed of four distinct phases: G1, S, G2 and M. To preserve cellular integrity, the cell has checkpoints which must be fulfilled in order to pass through each of the phase. Each of these checkpoints is regulated by a cyclin-CDK complex. The G2/M checkpoint is regulated by a Cyclin B1-CDK1 complex in the nucleus. In late G2 phase, Cyclin B1 (CycB1) accumulates in the nucleus from the cytoplasm. The overexpression of CycB1 has been associated with tumor aggressiveness and, therefore, CycB1 may have the potential to be a new therapeutic target in many aggressive cancers. Tuberin is a tumor suppressor protein that can bind CycB1 in the cytoplasm to regulate entry of CycB1 into the nucleus during the G2/M transition. Research into the Tuberin and CycB1 interaction may be promising for the field of cancer research. The Porter lab has studied the Tuberin-CycB1 interaction in vitro using established cell lines, but no one to date has studied this using an in vivo model which would provide us with more in-depth information about disease models. This project focuses on validating the Drosophila melanogaster as a model to study the Tuberin-CycB1 interaction. Drosophila melanogaster offers the unique advantage of having short generation times to permit high-throughput data to be collected. Moreover, the imaginal discs in the eye and wing of Drosophila contain regions of cells that are synchronized in the various phases of the cell cycle, providing the advantage that results can be seen at every phase of the cell cycle using this system. Our goal for this project is to first develop and validate a Drosophila disease model for Tuberin-CycB1 interactions and use it to gain more insight on possible targeted treatments for cancer using CyclinB1.