One of the unique features of eukaryotic organisms is the ability to go through meiosis, a specialized division that yields gametes for sexual reproduction. The ability to enter meiosis is precisely regulated: it is generally restricted to particular tissues, types of cells, or environments.
Our aim i s to understand the mechanisms that govern the decision to enter meiosis in the budding yeast, Saccharomyces cerevisiae. These studies will identify gene products and regulatory mechanisms that may have counterparts in other eukaryotes. The long-term result of our studies will be elucidation of genes and mechanisms that govern meiosis in other eukaryotes, including Man. A detailed picture has emerged of the genetic control of meiosis in yeast. Meiosis is restricted to one type of cell, the a/alpha cell, and is induced by starvation. The cell type signal is transmitted by the RME1 gene, which specifies a DNA-binding protein that inhibits meiosis. Both cell type and nutritional signals are transmitted by the IME1 gene, which specifies a nuclear protein that stimulates meiosis, and by the IME2 gene, which specifies a protein kinase homolog that also stimulates meiosis. Expression of IME1 increases in response to starvation; the IME1 product stimulates expression of IME2 and many other meiotic genes. The IME2 product then further activates many of the same meiotic genes and simultaneously shuts IME1 off. The RME1 product inhibits meiosis by blocking expression of IME1; RME1 is repressed in a/alpha cells, which enables them to enter meiosis. Our goal is to determine the mechanisms by which RME1, IME1, and IME2 products govern each other's expression.
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