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Download or read book Regulation of Meiotic Commitment in Saccharomyces Cerevisiae written by Olivia Hamill Ballew and published by . This book was released on 2020 with total page 159 pages. Available in PDF, EPUB and Kindle. Book excerpt: Cell division is fundamental for the development and function of all living organisms. There are two main mechanisms to divide a cell- meiosis and mitosis. Meiosis is the cell division process needed to produce gametes, whereas mitosis produces somatic cells. Although cells most often faithfully divide, the processes of meiosis and mitosis are not completely error free. Checkpoints are surveillance mechanisms in cells that sense errors and delay cell division, allowing the cell time to correct errors.Once meiosis has initiated, many organisms pass an irreversible transition point at which they commit to meiotic divisions. It is imperative that the cell completes meiosis faithfully to prevent aberrant chromosome segregation. How cells remain committed to the process of meiosis remains poorly understood. In my thesis, I addressed mechanisms underlying meiotic commitment. In budding yeast, meiosis is initiated in response to the absence of nutrients, and the commitment point occurs during prometaphase I. If cells are given nutrients before prometaphase I, they will abort meiosis, bud, and return to mitotic divisions. After prometaphase I, cells will remain committed to meiosis even in the presence of nutrients. I investigated the role of cell-cycle checkpoints in regulating meiotic commitment. I discovered novel roles for two checkpoints in ensuring meiotic commitment in budding yeast. I found that the DNA damage checkpoint and the spindle position checkpoint function in meiosis to ensure that cells remain committed to meiosis in the presence of nutrients. In the absences of these two checkpoints, cells inappropriately abort the meiotic program and return to mitotic growth, forming multinucleate polyploid cells. Interestingly, neither of these checkpoints has a previously reported role in meiosis I. Additionally, I investigated how cells adapt to increased aneuploidy in mitosis. Aneuploidy is defined as a loss or gain of one or more chromosomes. I deleted BUB3, a gene that encodes a protein involved in kinetochore-microtubule error correction and the spindle checkpoint, consequently increasing chromosome mis-segregation. Cells without a functional copy of BUB3 accumulated additional copies of specific chromosomes. I propose the complex karyotype suppresses negative effects normally associated with aneuploidy. These results are impactful to the field of chromosome integrity, providing insight into how cells prevent errors during cell division.