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Plk1 Spatial Synchronization in Prostate Epithelial Cells During Mitosis


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Cell division is a process whereby genetic material is duplicated, separated, and packaged to yield two daughter cells. This process relies on spatial and temporal synchronization of protein kinase activity at the mitotic spindle, a macromolecular machine that segregates chromosomes towards the daughter cells. A major generator of this machine and organizer of mitotic signaling is the centrosome. Interphase cells have a single centrosome that nucleates microtubules for cellular material to transport on. When cells decide to divide into two, they duplicate their genetic material and their centrosomes to make two mitotic spindle poles, which function to nucleate microtubules to capture duplicated genetic material and distribute it equally to each daughter cell. We propose a testable model that defects in centrosome number and function lead to genomic instability causing a normal prostate epithelial cell genome to behave like a cancer genome. To test this, we are determining the mechanism of centrosome amplification in prostate cancer cells and its impact on genome stability. Our studies will address the overall hypothesis that deregulation of centrosome based signaling events leads to genomic instability and subsequent metastasis in prostate cancer.



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