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Reference: Mitchell AP (1994) Control of meiotic gene expression in Saccharomyces cerevisiae. Microbiol Rev 58(1):56-70

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Abstract

Sporulation of the yeast Saccharomyces cerevisiae is restricted to one type of cell, the a/alpha cell, and is initiated after starvation for nitrogen in the absence of a fermentable carbon source. More than 25 characterized genes are expressed only during sporulation and are referred to as meiotic genes or sporulation-specific genes. These genes are in the early, middle, and late expression classes. Most early genes have a 5' regulatory site, URS1, and one of two additional sequences, UASH or a T4C site. URS1 is required both to repress meiotic genes during vegetative growth and to activate these genes during meiosis. UASH and the T4C site also contribute to meiotic expression. A different type of site, the NRE, is found in at least two late genes. The NRE behaves as a repression site in vegetative cells and is neutral in meiotic cells. Many regulatory genes that either repress or activate meiotic genes have been identified. One group of regulators affects the expression of IME1, which specifies a positive regulator of meiotic genes and is expressed at the highest levels in meiotic cells. A second group of regulators acts in parallel with or downstream of IME1 to influence meiotic gene expression. This group includes UME6, which is required both for repression through the URS1 site in vegetative cells and for IME1-dependent activation of an upstream region containing URS1 and T4C sites. IME1 may activate meiotic genes by modifying a UME6-dependent repression complex at a URS1 site. Several additional mechanisms restrict functional expression of some genes to meiotic cells. Translation of IME1 has been proposed to occur only in meiotic cells; several meiotic transcripts are more stable in acetate medium than in glucose medium; and splicing of MER2 RNA depends on a meiosis-specific gene, MER1.

Reference Type
Journal Article | Review | Research Support, Non-U.S. Gov't | Research Support, U.S. Gov't, P.H.S.
Authors
Mitchell AP
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